Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.
The external, nonvascular layer of the skin. It is made up, from within outward, of five layers of EPITHELIUM: (1) basal layer (stratum basale epidermidis); (2) spinous layer (stratum spinosum epidermidis); (3) granular layer (stratum granulosum epidermidis); (4) clear layer (stratum lucidum epidermidis); and (5) horny layer (stratum corneum epidermidis).
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
A type I keratin that is found associated with the KERATIN-1 in terminally differentiated epidermal cells such as those that form the stratum corneum. Mutations in the genes that encode keratin-10 have been associated with HYPERKERATOSIS, EPIDERMOLYTIC.
A type I keratin that is found associated with the KERATIN-5 in the internal stratified EPITHELIUM. Mutations in the gene for keratin-14 are associated with EPIDERMOLYSIS BULLOSA SIMPLEX.
Restoration of integrity to traumatized tissue.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Any inflammation of the skin.
Synthetic material used for the treatment of burns and other conditions involving large-scale loss of skin. It often consists of an outer (epidermal) layer of silicone and an inner (dermal) layer of collagen and chondroitin 6-sulfate. The dermal layer elicits new growth and vascular invasion and the outer layer is later removed and replaced by a graft.
A tube-like invagination of the EPIDERMIS from which the hair shaft develops and into which SEBACEOUS GLANDS open. The hair follicle is lined by a cellular inner and outer root sheath of epidermal origin and is invested with a fibrous sheath derived from the dermis. (Stedman, 26th ed) Follicles of very long hairs extend into the subcutaneous layer of tissue under the SKIN.
Tumors or cancer of the SKIN.
Mammalian pigment cells that produce MELANINS, pigments found mainly in the EPIDERMIS, but also in the eyes and the hair, by a process called melanogenesis. Coloration can be altered by the number of melanocytes or the amount of pigment produced and stored in the organelles called MELANOSOMES. The large non-mammalian melanin-containing cells are called MELANOPHORES.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The functions of the skin in the human and animal body. It includes the pigmentation of the skin.
Products of viral oncogenes, most commonly retroviral oncogenes. They usually have transforming and often protein kinase activities.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Established cell cultures that have the potential to propagate indefinitely.
ONCOGENE PROTEINS from papillomavirus that deregulate the CELL CYCLE of infected cells and lead to NEOPLASTIC CELL TRANSFORMATION. Papillomavirus E7 proteins have been shown to interact with various regulators of the cell cycle including RETINOBLASTOMA PROTEIN and certain cyclin-dependent kinase inhibitors.
A family of small, non-enveloped DNA viruses infecting birds and most mammals, especially humans. They are grouped into multiple genera, but the viruses are highly host-species specific and tissue-restricted. They are commonly divided into hundreds of papillomavirus "types", each with specific gene function and gene control regions, despite sequence homology. Human papillomaviruses are found in the genera ALPHAPAPILLOMAVIRUS; BETAPAPILLOMAVIRUS; GAMMAPAPILLOMAVIRUS; and MUPAPILLOMAVIRUS.
Lining of the ORAL CAVITY, including mucosa on the GUMS; the PALATE; the LIP; the CHEEK; floor of the mouth; and other structures. The mucosa is generally a nonkeratinized stratified squamous EPITHELIUM covering muscle, bone, or glands but can show varying degree of keratinization at specific locations.
The double-layered skin fold that covers the GLANS PENIS, the head of the penis.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A layer of vascularized connective tissue underneath the EPIDERMIS. The surface of the dermis contains innervated papillae. Embedded in or beneath the dermis are SWEAT GLANDS; HAIR FOLLICLES; and SEBACEOUS GLANDS.
A type of junction that attaches one cell to its neighbor. One of a number of differentiated regions which occur, for example, where the cytoplasmic membranes of adjacent epithelial cells are closely apposed. It consists of a circular region of each membrane together with associated intracellular microfilaments and an intercellular material which may include, for example, mucopolysaccharides. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990; Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Transglutaminases catalyze cross-linking of proteins at a GLUTAMINE in one chain with LYSINE in another chain. They include keratinocyte transglutaminase (TGM1 or TGK), tissue transglutaminase (TGM2 or TGC), plasma transglutaminase involved with coagulation (FACTOR XIII and FACTOR XIIIa), hair follicle transglutaminase, and prostate transglutaminase. Although structures differ, they share an active site (YGQCW) and strict CALCIUM dependence.
A circumscribed benign epithelial tumor projecting from the surrounding surface; more precisely, a benign epithelial neoplasm consisting of villous or arborescent outgrowths of fibrovascular stroma covered by neoplastic cells. (Stedman, 25th ed)
Melanin-containing organelles found in melanocytes and melanophores.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Mutant strains of mice that produce little or no hair.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
A fibroblast growth factor that is a specific mitogen for EPITHELIAL CELLS. It binds a complex of HEPARAN SULFATE and FIBROBLAST GROWTH FACTOR RECEPTOR 2B.
Adherence of cells to surfaces or to other cells.
A desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS VULGARIS.
An anchoring junction of the cell to a non-cellular substrate, similar in morphology to halves of DESMOSOMES. They are composed of specialized areas of the plasma membrane where INTERMEDIATE FILAMENTS bind on the cytoplasmic face to the transmembrane linkers, INTEGRINS, via intracellular attachment proteins, while the extracellular domain of the integrins binds to EXTRACELLULAR MATRIX PROTEINS.
Visible accumulations of fluid within or beneath the epidermis.
A filament-like structure consisting of a shaft which projects to the surface of the SKIN from a root which is softer than the shaft and lodges in the cavity of a HAIR FOLLICLE. It is found on most surfaces of the body.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A chronic inflammatory genetically determined disease of the skin marked by increased ability to form reagin (IgE), with increased susceptibility to allergic rhinitis and asthma, and hereditary disposition to a lowered threshold for pruritus. It is manifested by lichenification, excoriation, and crusting, mainly on the flexural surfaces of the elbow and knee. In infants it is known as infantile eczema.
Filaments 7-11 nm in diameter found in the cytoplasm of all cells. Many specific proteins belong to this group, e.g., desmin, vimentin, prekeratin, decamin, skeletin, neurofilin, neurofilament protein, and glial fibrillary acid protein.
Agents that soften, separate, and cause desquamation of the cornified epithelium or horny layer of skin. They are used to expose mycelia of infecting fungi or to treat corns, warts, and certain other skin diseases.
A type II keratin that is found associated with the KERATIN-10 in terminally differentiated epidermal cells such as those that form the stratum corneum. Mutations in the genes that encode keratin-1 have been associated with HYPERKERATOSIS, EPIDERMOLYTIC.
Small, sacculated organs found within the DERMIS. Each gland has a single duct that emerges from a cluster of oval alveoli. Each alveolus consists of a transparent BASEMENT MEMBRANE enclosing epithelial cells. The ducts from most sebaceous glands open into a HAIR FOLLICLE, but some open on the general surface of the SKIN. Sebaceous glands secrete SEBUM.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
DEFENSINS found mainly in epithelial cells.
A family of structurally-related short-chain collagens that do not form large fibril bundles.
Coloration of the skin.
The grafting of skin in humans or animals from one site to another to replace a lost portion of the body surface skin.
Also known as CD104 antigen, this protein is distinguished from other beta integrins by its relatively long cytoplasmic domain (approximately 1000 amino acids vs. approximately 50). Five alternatively spliced isoforms have been described.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
Separation of the prickle cells of the stratum spinosum of the epidermis, resulting in atrophy of the prickle cell layer. It is seen in diseases such as pemphigus vulgaris (see PEMPHIGUS) and DARIER DISEASE.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Recirculating, dendritic, antigen-presenting cells containing characteristic racket-shaped granules (Birbeck granules). They are found principally in the stratum spinosum of the EPIDERMIS and are rich in Class II MAJOR HISTOCOMPATIBILITY COMPLEX molecules. Langerhans cells were the first dendritic cell to be described and have been a model of study for other dendritic cells (DCs), especially other migrating DCs such as dermal DCs and INTERSTITIAL DENDRITIC CELLS.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
A form of epidermolysis bullosa characterized by serous bullae that heal without scarring. Mutations in the genes that encode KERATIN-5 and KERATIN-14 have been associated with several subtypes of epidermolysis bullosa simplex.
A type of ALPHAPAPILLOMAVIRUS especially associated with malignant tumors of the CERVIX and the RESPIRATORY MUCOSA.
One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.
Absence of hair from areas where it is normally present.
A short pro-domain caspase that is almost exclusively expressed in the EPIDERMIS and may play a role in the differentiation of epidermal KERATINOCYTES.
A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
7,12-Dimethylbenzanthracene. Polycyclic aromatic hydrocarbon found in tobacco smoke that is a potent carcinogen.
A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
An autosomal dominantly inherited skin disorder characterized by recurrent eruptions of vesicles and BULLAE mainly on the neck, axillae, and groin. Mutations in the ATP2C1 gene (encoding the secretory pathway Ca2++/Mn2++ ATPase 1 (SPCA1)) cause this disease. It is clinically and histologically similar to DARIER DISEASE - both have abnormal, unstable DESMOSOMES between KERATINOCYTES and defective CALCIUM-TRANSPORTING ATPASES. It is unrelated to PEMPHIGUS VULGARIS though it closely resembles that disease.
Desmoplakins are cytoskeletal linker proteins that anchor INTERMEDIATE FILAMENTS to the PLASMA MEMBRANE at DESMOSOMES.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A type I keratin found in the basal layer of the adult epidermis and in other stratified epithelia.
A type I keratin found associated with KERATIN-6 in rapidly proliferating squamous epithelial tissue. Mutations in the gene for keratin-17 have been associated with PACHYONYCHIA CONGENITA, TYPE 2.
Form of epidermolysis bullosa having onset at birth or during the neonatal period and transmitted through autosomal recessive inheritance. It is characterized by generalized blister formation, extensive denudation, and separation and cleavage of the basal cell plasma membranes from the basement membrane.
A type II keratin that is found associated with the KERATIN-14 in the internal stratified EPITHELIUM. Mutations in the gene for keratin-5 are associated with EPIDERMOLYSIS BULLOSA SIMPLEX.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
An integrin alpha subunit that primarily associates with INTEGRIN BETA1 or INTEGRIN BETA4 to form laminin-binding heterodimers. Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their cytoplasmic domains and are regulated in a tissue-specific and developmental stage-specific manner.
A chronic, congenital ichthyosis inherited as an autosomal recessive trait. Infants are usually born encased in a collodion membrane which sheds within a few weeks. Scaling is generalized and marked with grayish-brown quadrilateral scales, adherent at their centers and free at the edges. In some cases, scales are so thick that they resemble armored plate.
Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release.
A group of desmosomal cadherins with cytoplasmic tails that resemble those of classical CADHERINS.
The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight.
A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Methods for maintaining or growing CELLS in vitro.
A contact dermatitis due to allergic sensitization to various substances. These substances subsequently produce inflammatory reactions in the skin of those who have acquired hypersensitivity to them as a result of prior exposure.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.

Differential regulation of the human nidogen gene promoter region by a novel cell-type-specific silencer element. (1/6758)

Transfection analyses of the human nidogen promoter region in nidogen-producing fibroblasts from adult skin revealed multiple positive and negative cis-acting elements controlling nidogen gene expression. Characterization of the positive regulatory domains by gel mobility-shift assays and co-transfection studies in Drosophila SL2 cells unequivocally demonstrated that Sp1-like transcription factors are essential for a high expression of the human nidogen gene. Analysis of the negative regulatory domains identified a novel silencer element between nt -1333 and -1322, which is bound by a distinct nuclear factor, by using extracts from adult but not from embryonal fibroblasts. In embryonal fibroblasts, which express significantly higher amounts of nidogen mRNA as compared with adult fibroblasts, this inhibitory nidogen promoter region did not affect nidogen and SV40 promoter activities. The silencer element seems to be active only in nidogen-producing cells. Therefore this regulatory element might function in vivo to limit nidogen gene expression in response to external stimuli. However, none of the identified regulatory elements, including the silencer, contribute significantly to cell-specific expression of the human nidogen gene. Instead we provide evidence that gene expression in epidermal keratinocytes that are not producing nidogen is repressed by methylation-specific and chromatin-dependent mechanisms.  (+info)

The integrin alpha v beta 6 binds and activates latent TGF beta 1: a mechanism for regulating pulmonary inflammation and fibrosis. (2/6758)

Transforming growth factor beta (TGF beta) family members are secreted in inactive complexes with a latency-associated peptide (LAP), a protein derived from the N-terminal region of the TGF beta gene product. Extracellular activation of these complexes is a critical but incompletely understood step in regulation of TGF beta function in vivo. We show that TGF beta 1 LAP is a ligand for the integrin alpha v beta 6 and that alpha v beta 6-expressing cells induce spatially restricted activation of TGF beta 1. This finding explains why mice lacking this integrin develop exaggerated inflammation and, as we show, are protected from pulmonary fibrosis. These data identify a novel mechanism for locally regulating TGF beta 1 function in vivo by regulating expression of the alpha v beta 6 integrin.  (+info)

Murine matrix metalloproteinase 9 gene. 5'-upstream region contains cis-acting elements for expression in osteoclasts and migrating keratinocytes in transgenic mice. (3/6758)

Knowledge about the regulation of cell lineage-specific expression of extracellular matrix metalloproteinases is limited. In the present work, the murine matrix metalloproteinase 9 (MMP-9) gene was shown to contain 13 exons, and the 2.8-kilobase pair upstream region was found to contain several common promoter elements including a TATA box-like motif, three GC boxes, four AP-1-like binding sites, an AP-2 site, and three PEA3 consensus sequences that may be important for basic activity of the gene. In order to identify cell-specific regulatory elements, constructs containing varying lengths of the upstream region in front of a LacZ reporter gene were made and studied for expression in transgenic mice generated by microinjection into fertilized oocytes. Analyses of the mice revealed that the presence of sequences between -2722 and -7745 allowed for expression in osteoclasts and migrating keratinocytes, i. e. cells that have been shown to normally express the enzyme in vivo. The results represent the first in vivo demonstration of the location of cell-specific control elements in a matrix metalloproteinase gene and show that element(s) regulating most cell-specific activities of 92-kDa type collagenase are located in the -2722 to -7745 base pair region.  (+info)

The L1 major capsid protein of human papillomavirus type 11 recombinant virus-like particles interacts with heparin and cell-surface glycosaminoglycans on human keratinocytes. (4/6758)

The L1 major capsid protein of human papillomavirus (HPV) type 11, a 55-kDa polypeptide, forms particulate structures resembling native virus with an average particle diameter of 50-60 nm when expressed in the yeast Saccharomyces cerevisiae. We show in this report that these virus-like particles (VLPs) interact with heparin and with cell-surface glycosaminoglycans (GAGs) resembling heparin on keratinocytes and Chinese hamster ovary cells. The binding of VLPs to heparin is shown to exhibit an affinity comparable to that of other identified heparin-binding proteins. Immobilized heparin chromatography and surface plasmon resonance were used to show that this interaction can be specifically inhibited by free heparin and dextran sulfate and that the effectiveness of the inhibitor is related to its molecular weight and charge density. Sequence comparison of nine human L1 types revealed a conserved region of the carboxyl terminus containing clustered basic amino acids that bear resemblance to proposed heparin-binding motifs in unrelated proteins. Specific enzymatic cleavage of this region eliminated binding to both immobilized heparin and human keratinocyte (HaCaT) cells. Removal of heparan sulfate GAGs on keratinocytes by treatment with heparinase or heparitinase resulted in an 80-90% reduction of VLP binding, whereas treatment of cells with laminin, a substrate for alpha6 integrin receptors, provided minimal inhibition. Cells treated with chlorate or substituted beta-D-xylosides, resulting in undersulfation or secretion of GAG chains, also showed a reduced affinity for VLPs. Similarly, binding of VLPs to a Chinese hamster ovary cell mutant deficient in GAG synthesis was shown to be only 10% that observed for wild type cells. This report establishes for the first time that the carboxyl-terminal portion of HPV L1 interacts with heparin, and that this region appears to be crucial for interaction with the cell surface.  (+info)

C5a receptor and interleukin-6 are expressed in tissue macrophages and stimulated keratinocytes but not in pulmonary and intestinal epithelial cells. (5/6758)

The anaphylatoxin derived from the fifth component of the human complement system (C5a) mediates its effects by binding to a single high-affinity receptor (C5aR/CD88), the expression of which has been traditionally thought to be restricted to granulocytes, monocytes, macrophages (Mphi), and cell lines of myeloid origin. Recent immunohistochemical data suggested that human bronchial and alveolar cells express C5aR as well. To reexamine the tissue distribution of human C5aR expression, transcription of the C5aR gene was investigated in normal and pathologically affected human lung (bronchopneumonia, tuberculosis), large intestine (acute appendicitis, Crohn's disease), and skin (pyogenic granuloma, lichen planus) using in situ hybridization. In contrast to previous evidence, C5aR mRNA could not be detected in pulmonary or intestinal epithelial cells, whereas keratinocytes in inflamed but not in normal skin revealed detectable levels of C5aR transcripts. Additionally, it could be documented that only migrating Mphi express C5aR mRNA, whereas sessile Mphi in normal tissues and epithelioid/multinucleated Mphi found in granulomatous lesions do not. Because C5a has been demonstrated to upregulate the expression of interleukin (IL)-6 in human monocytes, we also studied IL-6 gene transcription in parallel to the C5aR. IL-6 mRNA was detectable in many tissue Mphi. Surprisingly, a tight co-expression of C5aR and IL-6 mRNA was observed in keratinocytes from lesions of pyogenic granuloma and lichen planus. These results point to an as yet unknown role for C5a in the pathogenesis of skin disorders beyond its well-defined function as a chemoattractant and activator of leukocytes.  (+info)

CCAAT/enhancer-binding proteins. A role in regulation of human involucrin promoter response to phorbol ester. (6/6758)

The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) is a potent inducer of keratinocyte differentiation and of involucrin gene expression. In the present study we show that a CCAAT/enhancer-binding protein (C/EBP) site in the proximal regulatory region is required for the phorbol ester response. Mutation of the C/EBP site results in the loss of basal and TPA-responsive activity. Gel mobility supershift analysis shows that C/EBPalpha binding to this site is increased by TPA treatment. Moreover, cotransfection of the human involucrin reporter plasmid with C/EBPalpha increases promoter activity to an extent comparable with TPA treatment. Mutation of the C/EBP-binding site eliminates these responses. Transfection experiments using GADD153 to create C/EBP-null conditions confirm that C/EBP factors are absolutely required for promoter activity and TPA responsiveness. C/EBPbeta and C/EBPdelta inhibit both TPA- and C/EBPalpha-dependent promoter activation, indicating functional differences among C/EBP family members. These results suggest that C/EBP transcription factor activity is necessary for basal promoter activity and TPA response of the involucrin gene.  (+info)

UV-A-induced decrease in nuclear factor-kappaB activity in human keratinocytes. (7/6758)

Previous reports have demonstrated an increase in nuclear factor-kappaB (NF-kappaB) activity in response to UV radiation. These studies have essentially focused on the DNA-damaging fraction of solar UV radiation (UV-B and UV-C). In contrast, the effects of UV-A radiation (320-400 nm) on NF-kappaB are not well known. In this study, we present evidence that UV-A radiation induces a marked decrease in NF-kappaB DNA-binding activity in NCTC 2544 human keratinocytes. In addition, NCTC 2544 keratinocytes pretreated with UV-A fail to respond to NF-kappaB inducers. Moreover, UV-A radiation induces a decrease in NF-kappaB-driven luciferase reporter gene expression in NCTC 2544 keratinocytes. The expression of the gene encoding IkappaBalpha (IkappaB is the NF-kappaB inhibitor), which is closely associated with NF-kappaB activity, is also reduced (3-fold) upon UV-A treatment. Our results indicate that the UV-A-induced decrease in NF-kappaB DNA-binding activity is associated with a decrease in the levels of the p50 and p65 protein subunits. This is the first evidence that an oxidative stress, such as UV-A radiation, may induce a specific decrease in NF-kappaB activity in mammalian cells, probably through degradation of NF-kappaB protein subunits. These findings suggest that UV-A could modulate the NF-kappaB-dependent gene expression.  (+info)

Psoriatic keratinocytes show reduced IRF-1 and STAT-1alpha activation in response to gamma-IFN. (8/6758)

Psoriasis is a chronic inflammatory dermatosis characterized by hyperproliferative keratinocytes (KC). The skin lesions are infiltrated by T cells, which secrete gamma interferon (gamma-IFN) and are believed to be necessary to maintain the psoriatic phenotype. In normal KC, gamma-IFN is a potent inhibitor of proliferation, but proliferation of KC persists in psoriatic plaques despite the presence of gamma-IFN. Immunostaining of interferon regulatory factor-1 (IRF-1) revealed that IRF-1 was localized to the basal cells of the epidermis in normal and in nonlesional psoriatic skin, but was suprabasal or completely absent in lesional psoriatic skin. This finding led to the hypothesis that abnormal signaling in the gamma-IFN pathway may occur in psoriatic KC. To test this hypothesis, we measured activation of IRF-1 and signal transducer and activator of transcription (STAT)-1alpha transcription factors in KC after stimulation with gamma-IFN. Primary cultures of KC from normal and nonlesional psoriatic skin were stimulated with gamma-IFN and subsequent transcription factor activation was measured by electrophoretic mobility shift assay. Psoriatic KC showed a reduced induction of IRF-1 and STAT-1alpha activation after stimulation with gamma-IFN, compared with normal KC. Reduced activation of IRF-1 and STAT-1alpha in response to gamma-IFN indicates a fundamental defect in the growth and differentiation control of psoriatic KC in the absence of the influence of other cell types.  (+info)

Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.

There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.

Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.

Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.

There are several types of dermatitis, including:

1. Atopic dermatitis: a chronic condition characterized by dry, itchy skin and a tendency to develop allergies.
2. Contact dermatitis: a localized reaction to an allergen or irritant that comes into contact with the skin.
3. Seborrheic dermatitis: a condition characterized by redness, itching, and flaking skin on the scalp, face, or body.
4. Psoriasis: a chronic condition characterized by thick, scaly patches on the skin.
5. Cutaneous lupus erythematosus: a chronic autoimmune disorder that can cause skin rashes and lesions.
6. Dermatitis herpetiformis: a rare condition characterized by itchy blisters or rashes on the skin.

Dermatitis can be diagnosed through a physical examination, medical history, and sometimes laboratory tests such as patch testing or biopsy. Treatment options for dermatitis depend on the cause and severity of the condition, but may include topical creams or ointments, oral medications, phototherapy, or lifestyle changes such as avoiding allergens or irritants.

There are several types of skin neoplasms, including:

1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.

While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.

Some common types of skin diseases include:

1. Acne: a condition characterized by oil clogged pores, pimples, and other blemishes on the skin.
2. Eczema: a chronic inflammatory skin condition that causes dry, itchy, and scaly patches on the skin.
3. Psoriasis: a chronic autoimmune skin condition characterized by red, scaly patches on the skin.
4. Dermatitis: a term used to describe inflammation of the skin, often caused by allergies or irritants.
5. Skin cancer: a type of cancer that affects the skin cells, often caused by exposure to UV radiation from the sun or tanning beds.
6. Melanoma: the most serious type of skin cancer, characterized by a mole that changes in size, shape, or color.
7. Vitiligo: a condition in which white patches develop on the skin due to the loss of pigment-producing cells.
8. Alopecia: a condition characterized by hair loss, often caused by autoimmune disorders or genetics.
9. Nail diseases: conditions that affect the nails, such as fungal infections, brittleness, and thickening.
10. Mucous membrane diseases: conditions that affect the mucous membranes, such as ulcers, inflammation, and cancer.

Skin diseases can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or blood tests. Treatment options vary depending on the specific condition and may include topical creams or ointments, oral medications, light therapy, or surgery.

Preventive measures to reduce the risk of skin diseases include protecting the skin from UV radiation, using sunscreen, wearing protective clothing, and avoiding exposure to known allergens or irritants. Early detection and treatment can help prevent complications and improve outcomes for many skin conditions.

Papillomas can occur anywhere on the body, but they are most commonly found on the face, neck, and scalp. They may appear as small bumps or growths that look like a wart. In some cases, papillomas may be associated with human papillomavirus (HPV) infection.

Papillomas are typically diagnosed through a physical examination of the affected area. In some cases, a biopsy may be performed to confirm the diagnosis and rule out other potential causes. Treatment for papillomas usually involves removal of the growth through a minor surgical procedure or cryotherapy (freezing).

Papillomas are not cancerous and do not typically pose any long-term health risks. However, they may be unsightly and can cause psychological distress for some people. In these cases, treatment may be sought for cosmetic reasons. It is important to note that papillomas should not be confused with squamous cell carcinoma, a type of skin cancer that can resemble a papilloma in appearance but has the potential to be more aggressive and harmful.

There are several types of pemphigus, including:

1. Pemphigus vulgaris: This is the most common form of the disease and is characterized by the formation of large, painful blisters on the skin and mucous membranes.
2. Pemphigus foliaceus: This type of pemphigus is characterized by the formation of smaller, crusting sores on the skin.
3. Pemphigus erythematosus: This type of pemphigus is characterized by the formation of flat, red sores on the skin.
4. Bullous pemphigoid: This is a rare form of pemphigus that is characterized by the formation of large, fluid-filled blisters on the skin.

Treatment for pemphigus typically involves the use of corticosteroids and immunosuppressive drugs to reduce inflammation and suppress the immune system. In severe cases, hospitalization may be necessary to manage complications such as infection and fluid loss.

Prevention of pemphigus is difficult, but avoiding exposure to known triggers such as certain medications and taking steps to maintain good skin care can help reduce the risk of developing the disease. Early diagnosis and treatment are important to prevent complications and improve outcomes for patients with pemphigus.

Blisters are caused by friction or rubbing against a surface, which causes the top layer of skin to separate from the underlying layer. This separation creates a space that fills with fluid, forming a blister. Blisters can also be caused by burns, chemical exposure, or other types of injury.

There are different types of blisters, including:

1. Friction blisters: These are the most common type of blister and are caused by friction or rubbing against a surface. They are often seen on the hands, feet, and buttocks.
2. Burn blisters: These are caused by burns and can be more severe than friction blisters.
3. Chemical blisters: These are caused by exposure to chemicals and can be very painful.
4. Blisters caused by medical conditions: Certain medical conditions, such as epidermolysis bullosa (a genetic disorder that affects the skin), can cause blisters to form easily.

Blisters can be treated in several ways, depending on their size and location. Small blisters may not require treatment and can heal on their own within a few days. Larger blisters may need to be drained and covered with a bandage to prevent infection. In severe cases, surgical intervention may be necessary.

Preventing blisters is key to avoiding the discomfort and pain they can cause. To prevent blisters, it is important to:

1. Wear properly fitting shoes and clothing to reduce friction.
2. Use lubricating creams or powders to reduce friction.
3. Take regular breaks to rest and allow the skin to recover.
4. Avoid using harsh chemicals or detergents that can cause irritation.
5. Keep the affected area clean and dry to prevent infection.

In conclusion, blisters are a common and uncomfortable condition that can be caused by a variety of factors. While they can be treated and managed, prevention is key to avoiding the discomfort and pain they can cause. By taking steps to prevent blisters and seeking medical attention if they do occur, individuals can reduce their risk of developing this uncomfortable condition.

Also known as eczema or atopic eczema.

Dermatitis, Atopic is a common condition that affects people of all ages but is most prevalent in children. It is often associated with other atopic conditions such as asthma and allergies. The exact cause of dermatitis, atopic is not known, but it is thought to involve a combination of genetic and environmental factors.

Symptoms of Dermatitis, Atopic:

* Redness and dryness of the skin
* Scaling and flaking of the skin
* Itching and burning sensations
* Thickening and pigmentation of the skin
* Small blisters or weeping sores

Atopic dermatitis can occur anywhere on the body but is most commonly found on the face, neck, hands, and feet.

Treatment for Dermatitis, Atopic:

* Moisturizers to keep the skin hydrated and reduce dryness
* Topical corticosteroids to reduce inflammation
* Antihistamines to relieve itching
* Phototherapy with ultraviolet light
* Oral immunomodulators for severe cases

It is important to note that dermatitis, atopic is a chronic condition, and treatment should be ongoing. Flare-ups may occur, and adjustments to the treatment plan may be necessary.

Prevention of Dermatitis, Atopic:

* Avoiding triggers such as soaps, detergents, and stress
* Keeping the skin well-moisturized
* Avoiding extreme temperatures and humidity
* Wearing soft, breathable clothing
* Using mild cleansers and avoiding harsh chemicals

Early diagnosis and treatment of dermatitis, atopic can help improve the quality of life for those affected. It is important to work with a healthcare professional to develop an appropriate treatment plan and manage symptoms effectively.

SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.

SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.

Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.

Acantholysis is caused by a variety of factors, including genetic mutations, autoimmune disorders, and exposure to certain medications or chemicals. It can affect any area of the body, but it most commonly occurs on the skin of the face, neck, and hands.

The symptoms of acantholysis can vary depending on the underlying cause of the condition. Common symptoms include:

* Thin, fragile skin that is prone to tearing or breaking
* Formation of small, flat scars or lesions on the skin
* Skin that is sensitive to touch or pressure
* Redness and inflammation around the affected area

Acantholysis can be diagnosed through a combination of physical examination, medical history, and laboratory tests. Treatment for acantholysis depends on the underlying cause of the condition and may include topical medications, oral medications, or injectable treatments. In severe cases, surgery may be necessary to repair damaged skin tissue.

Preventing acantholysis can be challenging, but there are some steps that can help reduce the risk of developing the condition. These include:

* Avoiding exposure to harsh chemicals or medications
* Protecting the skin from excessive sun exposure and using sunscreen when necessary
* Using gentle skincare products and avoiding scrubbing or rubbing the skin excessively
* Managing underlying medical conditions, such as autoimmune disorders or hormonal imbalances, that can contribute to acantholysis.

Overall, acantholysis is a rare and complex condition that requires careful diagnosis and management to prevent complications and improve quality of life for individuals affected by the condition.

Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.

Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.

In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.

It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.

See also: Cancer, Tumor

Word count: 190

There are three main types of EBS, each with different severity and symptoms:

1. Epidermolysis Bullosa Simplex (EBS) - the mildest form, characterized by minor skin blistering and scarring.
2. Epidermolysis Bullosa Junctional (EBJ) - a more severe form, involving the skin and mucous membranes, with more extensive blistering and scarring.
3. Epidermolysis Bullosa Dystrophic (EBD) - the most severe form, with widespread blistering, scarring, and disfigurement, as well as a high risk of squamous cell carcinoma.

EBS is caused by mutations in one of several genes that are responsible for creating proteins important for skin strength and stability. The disorder is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition.

Treatment for EBS typically focuses on managing symptoms and preventing complications, such as infection and scarring. This may include:

1. Wound care - keeping wounds clean and covered to promote healing and prevent infection.
2. Pain management - using medication to manage pain associated with blistering and scarring.
3. Physical therapy - exercises and stretches to improve joint mobility and reduce the risk of contractures.
4. Phototherapy - exposure to specific wavelengths of light to help heal skin and reduce inflammation.
5. Surgery - in severe cases, surgery may be necessary to remove scar tissue or repair damaged skin.

There is currently no cure for EBS, but researchers are working to develop new treatments and therapies to improve quality of life for people with the disorder.

1. Alopecia areata: This is an autoimmune disorder that causes patchy hair loss on the scalp or body.
2. Androgenetic alopecia (male pattern baldness): This is a common condition in which men experience hair loss due to hormonal changes.
3. Telogen effluvium: This is a condition where there is an increase in the number of hair follicles that stop growing and enter the resting phase, leading to excessive hair shedding.
4. Alopecia totalis: This is a condition where all hair on the scalp is lost, including eyebrows and lashes.
5. Alopecia universalis: This is a condition where all body hair is lost.

Alopecia can be caused by a variety of factors, including genetics, hormonal imbalances, autoimmune disorders, and certain medications. Treatment options for alopecia depend on the underlying cause and may include medications, hair transplantation, or other therapies.

In medical literature, alopecia is often used as a term to describe the loss of hair in specific contexts, such as in the treatment of cancer patients or in the management of autoimmune disorders. It is also used to describe the side effects of certain medications, such as chemotherapy drugs that can cause hair loss.

The symptoms of BFP typically appear in early adulthood and can include:

* Blisters and sores on the skin and mucous membranes
* Pain and discomfort
* Scarring and disfigurement
* Difficulty swallowing (in severe cases)

BFP is diagnosed through a combination of clinical evaluation, family history, and genetic testing. Treatment for the condition typically involves managing the symptoms and preventing complications. This may include:

* Topical medications to reduce inflammation and promote healing
* Oral medications to suppress the immune system and prevent further blistering
* Physical therapy to improve mobility and reduce pain

While there is no cure for BFP, early diagnosis and appropriate treatment can help to manage the symptoms and improve quality of life. The condition is typically inherited in an autosomal dominant pattern, which means that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous mutations rather than inheritance.

Junctional EB (JEB) is a type of EB that affects the space between cells in the skin, known as the basement membrane zone. This condition is caused by mutations in the genes that encode proteins involved in the structure and function of the basement membrane.

Symptoms of JEB typically appear at birth or in early childhood and may include:

* Skin blisters and sores, often on the hands, feet, and other areas exposed to friction
* Thickening and scarring of the skin
* Delayed healing of wounds
* Skin cancer risk

JEB is diagnosed through a combination of clinical evaluation, genetic testing, and histopathological analysis of skin biopsies. There is no cure for JEB, but various treatments can help manage symptoms and prevent complications. These may include:

* Wound care and dressing
* Pain management with medication
* Physical therapy to maintain joint mobility and prevent contractures
* Surgery to remove scar tissue or repair damaged skin

The prognosis for JEB varies depending on the severity of the condition. Some individuals with mild forms of JEB may lead relatively normal lives, while those with more severe forms of the condition may experience significant disability and reduced life expectancy.

A rare inherited disorder characterized by thick, plate-like scales on the skin, especially on the limbs and torso. These scales can be darker or lighter than normal skin color and may crack and split, leading to infection and other complications. The condition is caused by mutations in the filaggrin gene and tends to run in families. Treatment includes topical medications, phototherapy, and systemic medications such as corticosteroids or retinoids. Also known as ichthyosis lamellar, this disorder affects approximately 1 in 185,000 people worldwide.

Note: Ichthyosis, Lamellar is a type of ichthyosis, a group of genetic disorders that affect the skin's ability to produce natural oils and cause dry, scaly skin.

The symptoms of dermatitis, allergic contact can vary depending on the severity of the reaction, but may include:

* Redness and swelling of the affected area
* Itching, burning, or stinging sensations
* Small blisters or hives
* Thickening or scaling of the skin
* Crusting or oozing of fluid

Dermatitis, allergic contact can be caused by a variety of substances, including:

* Metals, such as nickel, chrome, and mercury
* Plastics, such as latex and polyethylene
* Certain chemicals, such as perfumes, dyes, and preservatives
* Plant extracts, such as poison ivy or poison oak
* Insect bites or stings

The diagnosis of dermatitis, allergic contact is typically made through a combination of physical examination, medical history, and patch testing. Patch testing involves applying small amounts of potential allergens to the skin and observing for any signs of an allergic reaction over a period of time.

Treatment for dermatitis, allergic contact typically focuses on removing the allergen from the affected area and providing relief from symptoms. This may include:

* Avoiding exposure to the allergen
* Applying topical creams or ointments to reduce inflammation and itching
* Taking oral medications, such as antihistamines or corticosteroids, to reduce symptoms
* In severe cases, hospitalization may be necessary to manage the reaction.

Preventative measures for dermatitis, allergic contact include:

* Avoiding exposure to potential allergens
* Wearing protective clothing or gloves when handling suspected allergens
* Using hypoallergenic products and avoiding fragrances and dyes
* Performing patch testing before introducing new substances into the environment.

It is important to seek medical attention if symptoms persist or worsen over time, as dermatitis, allergic contact can lead to complications such as infection or scarring. Early diagnosis and treatment can help prevent these complications and improve outcomes for patients with this condition.

Since keratinocyte differentiation inhibits keratinocyte proliferation, factors that promote keratinocyte proliferation should ... Functional keratinocytes are needed for tympanic perforation healing. A sunburn cell is a keratinocyte with a pyknotic nucleus ... Within the epidermis keratinocytes are associated with other cell types such as melanocytes and Langerhans cells. Keratinocytes ... Basal cells in the basal layer (stratum basale) of the skin are sometimes referred to as basal keratinocytes. Keratinocytes ...
... enzymes serve to specifically catalyze the development of the cornified cell envelope, a defining ... The specific cross linkages formed by keratinocyte transglutaminase are between n^ε-(γ-glutamyl)lysine residues which develop ... A study on the mutation of keratinocyte transglutaminase (TGK) came to conclude that those affected with ichthyosis lamellaris ... Keratinocyte ENSG00000285348 GRCh38: Ensembl release 89: ENSG00000092295, ENSG00000285348 - Ensembl, May 2017 GRCm38: Ensembl ...
The keratinocyte growth factor (KGF), also known as FGF7, is a growth factor present in the epithelialization-phase of wound ... In this phase, keratinocytes are covering the wound, forming the epithelium. KGF is a small signaling molecule that binds to ... FGF10 is also known as "keratinocyte growth factor 2". Palifermin Rotolo S, Ceccarelli S, Romano F, Frati L, Marchese C, ... Angeloni A (2008). Maas S (ed.). "Silencing of Keratinocyte Growth Factor Receptor Restores 5-Fluorouracil and Tamoxifen ...
... skin keratinocytes; and virtually all types of multicellular tissues. Formyl peptide receptor GRCh38: Ensembl release 89: ...
... can distinguish human keratinocyte cells from their transient amplifying keratinocyte analogues. The identification of this ... Pellegrini, Graziella; De Luca, Michele (November 13, 2018). "Living with Keratinocytes". Stem Cell Reports. 11 (5): 1026-1033 ... "p63 identifies keratinocyte stem cells". Proceedings of the National Academy of Sciences. 98 (6): 3156-3161. doi:10.1073/pnas. ...
Papillomaviruses replicate exclusively in keratinocytes. Keratinocytes form the outermost layers of the skin, as well as some ... The differentiation of keratinocytes can be mimicked in vitro by exposing cultured keratinocytes to an air/liquid interface. ... Less-differentiated keratinocyte stem cells, replenished on the surface layer, are thought to be the initial target of ... Keratinocyte stem cells in the epithelial basement layer can maintain papillomavirus genomes for decades. The expression of the ...
As keratinocytes continue migrating, new epithelial cells must be formed at the wound edges to replace them and to provide more ... Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric ... Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact ... Proliferation behind migrating keratinocytes normally begins a few days after wounding and occurs at a rate that is 17 times ...
Some of which are keratinocytes. Accumulation of these cancer cells causes a microscopic focus of abnormal cells that are, at ... Clear-cell squamous cell carcinoma (also known as clear-cell carcinoma of the skin) is characterized by keratinocytes that ... is characterized by a tubular microscopic pattern and keratinocyte acantholysis. Basaloid squamous cell carcinoma is ...
Cirillo N, Prime SS (June 2011). "Keratinocytes synthesize and activate cortisol". Journal of Cellular Biochemistry. 112 (6): ... but research has shown that keratinocytes in human skin also produce cortisol. Prolonged topical steroid (TS) application ...
TGFβ1 is a growth inhibitor in human keratinocytes. Stimulation of the cultured human keratinocyte cell line, HaCaT, with TGFβ1 ... Yang Y, Gil M, Byun SM, Choi I, Pyun KH, Ha H (1996). "Transforming growth factor-beta1 inhibits human keratinocyte ... UV-irradiation of primary human keratinocytes yields the same results, namely a reduction of PTPkappa tyrosine phosphatase ... protein-tyrosine phosphatase kappa by ultraviolet irradiation activates epidermal growth factor receptor in human keratinocytes ...
Keratinocyte growth factor is a protein that in humans is encoded by the FGF7 gene. The protein encoded by this gene is a ... Aaronson SA, Bottaro DP, Miki T, Ron D, Finch PW, Fleming TP, Ahn J, Taylor WG, Rubin JS (1992). "Keratinocyte growth factor. A ... Post M, Souza P, Liu J, Tseu I, Wang J, Kuliszewski M, Tanswell AK (Oct 1996). "Keratinocyte growth factor and its receptor are ... Guo L, Degenstein L, Fuchs E (Jan 1996). "Keratinocyte growth factor is required for hair development but not for wound healing ...
1998). "Two forms of collagen XVII in keratinocytes. A full-length transmembrane protein and a soluble ectodomain". J. Biol. ... Collagen XVII is constitutively shed from the keratinocyte surface within NC16A domain by TACE (TNF-Alpha Converting Enzyme), ... "Two forms of collagen XVII in keratinocytes. A full-length transmembrane protein and a soluble ectodomain". J. Biol. Chem. 273 ... multiprotein complexes at the dermal-epidermal basement membrane zone that mediate adhesion of keratinocytes to the underlying ...
They also have a function in keratinocytes. They are also expressed on peripheral nerve terminals. These receptors play a role ...
Its expression is markedly increased in human keratinocytes following stimulation with interferon-gamma and its expression is ... August 2010). "Upregulation of cathepsin S in psoriatic keratinocytes". Experimental Dermatology. 19 (8): e80-e88. doi:10.1111/ ... elevated in psoriatic keratinocytes due to stimulation by proinflammatory factors. In contrast, cortical thymic epithelial ...
Keratinocytes are the cells found lower in the epidermis and specialize in holding the surrounding skin cells together. It is ... It appears that a certain type of immune cell (cytotoxic CD8+ T cell) is primarily responsible for keratinocyte death and ... CD8+ T cells then mediate keratinocyte cell death through release of a number of molecules, including perforin, granzyme B, and ... Histologically, early TEN shows scattered necrotic keratinocytes. In more advanced TEN, full thickness epidermal necrosis is ...
The tonofibrils go on to form the desmosomes, which allow for strong connections to form between adjacent keratinocytes. The ... This layer is composed of polyhedral keratinocytes. These are joined with desmosomes. Their spiny (Latin, spinosum) appearance ... although the actual keratinocytes begin in the stratum basale. They have large pale-staining nuclei as they are active in ...
Keratinocytes carry the melanosomes with them as they move towards the surface. Keratinocytes contribute to skin pigmentation ... Melanosomes along with the melanin they contain are transferred from melanocytes to keratinocytes when keratinocytes are low in ... 2010). "Keratinocytes in culture accumulate phagocytosed melanosomes in the perinuclear area". Pigment Cell Melanoma Res. 23 (1 ... The transfer of melanosomes to keratinocytes is a necessary condition for the visible pigmentation of the skin. Blocking this ...
October 2006). "Methylparaben potentiates UV-induced damage of skin keratinocytes". Toxicology. 227 (1-2): 62-72. doi:10.1016/j ...
Both proteins co-localize on basal keratinocytes surface. Collagen XXIII plays a role as a biomarker for detection and ...
The TRPV3 channel has wide tissue expression that is especially high in the skin (keratinocytes) but also in the brain. It ... June 2002). "A heat-sensitive TRP channel expressed in keratinocytes". Science. 296 (5575): 2046-9. doi:10.1126/science.1073140 ... Receptor Potential Vanilloid TRPV3 Channel by Natural Forsythoside B Attenuates Pruritus and Cytotoxicity of Keratinocytes". ...
... was localized in the cytoplasm of resting human keratinocytes in vitro. It has been shown to interact with the RAGE ... November 2003). "S100C/A11 is a key mediator of Ca(2+)-induced growth inhibition of human epidermal keratinocytes". The Journal ... January 2008). "S100A11, an dual mediator for growth regulation of human keratinocytes". Molecular Biology of the Cell. 19 (1 ... Sakaguchi M, Huh NH (October 2011). "S100A11, a dual growth regulator of epidermal keratinocytes". Amino Acids. 41 (4): 797-807 ...
Arredondo J, Chernyavsky AI, Webber RJ, Grando SA (December 2005). "Biological effects of SLURP-1 on human keratinocytes". The ...
"Senescence-associated genes in normal human oral keratinocytes". Experimental Cell Research. 287 (2): 272-81. doi:10.1016/S0014 ...
They demonstrated growing a coherent layer of keratinocytes. These spider silk nanomembranes have also been used to create a ...
Adams, JC; Watt, FM (1989). "Fibronectin inhibits the terminal differentiation of human keratinocytes". Nature. 340 (6231): 307 ... Zhu, AJ; Watt, FM (1999). "beta-catenin signalling modulates proliferative potential of human epidermal keratinocytes ... where she served as Head of the Keratinocyte Laboratory. From 2007 to 2012 she worked in Cambridge, where she helped to ...
Scott, G.; Leopardi, S.; Printup, S.; Madden, B. (2002). "Filopodia are conduits for melanosome transfer to keratinocytes". ... Melanosomes are also transferred by filopodia from melanocytes to keratinocytes. This transfer involves a classic filopodial ...
... s are keratinocytes in their last stage of differentiation. Keratinocytes in the stratum basale of the epidermis will ... Skin Epidermis (skin) Keratinocyte Elias PM (April 2007). "The skin barrier as an innate immune element". Seminars in ... During that migration keratinocytes will undergo multiple stages of differentiation to finally become corneocytes once they ... Corneocytes are keratinocytes without nuclei and cytoplasmic organelles. They contain a highly insoluble cornified envelope ...
Only keratinocytes expressed significant amounts of form 1. Little is known about the functional significance of this ...
Melanin is then transferred to keratinocytes in melanosomes. Nevus cells in the skin and oral mucosa also produce melanin. Oral ...
IL-36γ is most produced by keratinocytes. It activates NF-κB via interleukin 1 receptor-like 2 (IL-1Rrp2) and is specifically ... IL-36ra is highly expressed by keratinocytes, in psoriatic skin, placenta, uterus, brain, kidneys, monocytes, B-lymphocytes and ... It is produced by monocytes, macrophages, osteoblasts, keratinocytes. It is synthesized as an inactive precursor that is ... The intracellular form was found in fibroblasts, monocytes, neutrophils, keratinocytes and bronchial epithelial cells. IL-1ra ...
Collaborative study of candidate standards for keratinocyte growth factor / C. Jane Robinson ... [‎et al]‎  ...
Super-resolution image of primary human keratinocytes detecting keratin 75 (green), the inner nuclear membrane protein SUN2 ( ...
Collaborative study of candidate standards for keratinocyte growth factor / C. Jane Robinson ... [‎et al]‎  ...
2D3 and their interactions with 2-catenin to inhibit keratinocyte proliferation, while promoting keratinocyte differentiation ... In the keratinocyte the major coactivator complexes include the vitamin D interacting protein (DRIP) complex and the steroid ... We found that the DRIP complex is the main complex binding to VDR in the proliferating keratinocyte, whereas SRC3 and its ... Grant Abstract: Vitamin D Receptor Coactivators in Keratinocytes. Grant Number: 5R01AR050023-09. PI Name: Bikle. Project Title ...
FORESKIN KERATINOCYTE (NEONATAL) (UNII: ZJO8CP3Q2A) (FORESKIN KERATINOCYTE (NEONATAL) - UNII:ZJO8CP3Q2A) FORESKIN KERATINOCYTE ... GINTUIT- allogeneic cultured keratinocytes and fibroblasts in bovine collagen cellular sheet. Out of scope - Out of scope for ... GINTUIT- allogeneic cultured keratinocytes and fibroblasts in bovine collagen cellular sheet. To receive this label RSS feed. ... GINTUIT- allogeneic cultured keratinocytes and fibroblasts in bovine collagen cellular sheet. If this SPL contains inactivated ...
Keratinocyte cancer. Authoritative facts from DermNet New Zealand. ... A keratinocyte cancer is a malignant neoplasm formed from keratinocytes, either from basal cell keratinocytes or squamous cell ... How are keratinocyte cancers classified?. Keratinocyte cancers are cancers of the skin. They are classified as:. *Basal cell ... Who gets keratinocyte cancers?. Keratinocyte cancers are the most common form of skin cancer and the most common form of cancer ...
In this study, the impact of triclosan exposure on the skin barrier and keratinocyte function was investigated using a model of ... Exposure to the anti-microbial chemical triclosan disrupts keratinocyte function and skin integrity in a model of reconstructed ... Exposure to the antimicrobial chemical triclosan disrupts keratinocyte function and skin integrity in a model of reconstructed ...
To identify the epidermal initiating signals produced by DLX3-null keratinocytes, we performed acute deletion of DLX3 in adu … ... Epidermal-specific deletion of the homeobox transcription regulator DLX3 disrupts keratinocyte differentiation and results in ... DLX3-Dependent STAT3 Signaling in Keratinocytes Regulates Skin Immune Homeostasis Shreya Bhattacharya 1 , Jin-Chul Kim 1 , ... DLX3-Dependent STAT3 Signaling in Keratinocytes Regulates Skin Immune Homeostasis Shreya Bhattacharya et al. J Invest Dermatol. ...
Keratinocyte Basal Medium MCDB 153 (Powder). Cat# MBS653431. Supplier: MyBiosource. Available at Gentaur Genprice in 5 to 7 ... MBS653431 , Keratinocyte Basal Medium MCDB 153 (Powder) MyBiosource Culture Media MBS653431 , Keratinocyte Basal Medium MCDB ... Keratinocyte Basal Medium MCDB 153 (Powder) , MBS653431 , MyBiosource. Product Short Name: [Keratinocyte Basal Medium MCDB 153] ... MBS653431 , Keratinocyte Basal Medium MCDB 153 (Powder). Rating Required Select Rating. 1 star (worst). 2 stars. 3 stars ( ...
Various culture media are used to propagate keratinocytes (KCs) in vitro. The COVID-19 pandemic resulted in supply chain ... Keywords: KC, keratinocyte; KGM2, keratinocyte growth medium 2; KSFM, keratinocyte serum-free media; OCLN, occludin; TEER, ... Data are presented as median (Q1, Q3). D, day; KC, keratinocyte; KGM2, keratinocyte growth medium 2; KSFM, keratinocyte serum- ... Data are presented as median (Q1, Q3). D, day; KGM2, keratinocyte growth medium 2; KSFM, keratinocyte serum-free media; MOI, ...
Biogeographic and disease-specific alterations in epidermal lipid composition and single-cell analysis of acral keratinocytes. ... Biogeographic and disease-specific alterations in epidermal lipid composition and single-cell analysis of acral keratinocytes. ... and we used single-cell RNA-Seq to compare keratinocyte gene expression at acral and nonacral sites. We demonstrate that acral ...
The MSDS of Keratinocyte for Basal is available from Karlan upon request. ... Keratinocyte Basal Medium MCDB 153 w/o Methionine, Cysteine, Calcium Culture Media 10 L - 1 kit is backordered and will ship as ... Keratinocyte Basal Medium MCDB 153 w/o Methionine, Cysteine, Calcium Culture Media 10 L ... Keratinocyte Basal Medium MCDB 153 w/o Methionine, Cysteine, Calcium Culture Media 10 L. ...
PRENATAL ARSENIC EXPOSURE ALTERS KERATINOCYTE STEM CELLS FATE AND INDUCES SKIN TUMORS WITH HIGHER MALIGNANT POTENTIAL. ... R03 proposal is to establish a scientific basis to understand the effect of transplacental arsenic exposure on keratinocyte ...
A method for repairing DNA damage in human keratinocytes by applying to the keratinocytes a composition comprising at least one ... Treated keratinocytes were incubated at 37° C. in 5% CO2. After 24 hours, cells were aspirated and keratinocytes were washed ... demonstrates that keratinocytes survival and viability are improved when keratinocytes are treated with the composition of the ... Normal human keratinocytes (HEKn) were cultured in Epilife® Medium with Human Keratinocyte Growth Supplement. The cells were ...
This normal human skin cell was treated with a growth factor that triggered the formation of specialized protein structures that enable the cell to move. We depend on cell movement for such basic functions as wound healing and launching an immune response.. Back to main page ...
All What Women Need For Their Beauty
Rapamycin retards epigenetic ageing of keratinocytes independently of its effects on replicative senescence, proliferation and ...
Posts about keratinocytes written by Mireia Ramos Muntada ... agingcáncerdermisdnaepidermishypodermisinfraredkeratinocytes ... Arxiu detiquetes: keratinocytes CONTENTS, ENGLISH, General, GENETICS White, brown or red?. 09/07/2017. Mireia Ramos Muntada ... Figure 1. Melanin (arrows) rising towards the keratinocytes (Source: Salud del Siglo XXI). Tan is the synthesis of new melanin ... The skin has two basic cells: keratinocytes (80%) and melanocytes (10%). The melanin, which gives the tan, is found inside the ...
Probiotic Adhesion to Skin Keratinocytes and Underlying Mechanisms. Probiotic Adhesion to Skin Keratinocytes and Underlying ... These showed that Escherichia coli is not able to invade skin keratinocytes, but adhered to them. Lacticaseibacillus rhamnosus ... Probiotic bacteria seem to use carbohydrates to adhere to the keratinocytes, while S. aureus uses proteins. Lacticaseibacillus ... In this study, invasion and adhesion studies have been carried out using keratinocytes. ...
a Representative images of keratinocytes at the end point of the migration assay using primary keratinocytes from WT or cKO ... Primary keratinocyte isolation and culturing. Primary keratinocytes were isolated through dispase and trypsin cell dissociation ... we found keratinocytes lacking either Sox11 or Sox4 migrated at a similar rate to that of wild-type keratinocytes, whereas ... dcKO keratinocytes were transduced to express luciferase (Luc, control), Sox11, Sox4, or both Sox11 and Sox4. Graph quantifying ...
Identifies keratinocyte of growth factors, i.e. embryonic development, cell growth, morphogenesis, tumor growth,and invasion ... Discovered recombinant DNA technology to produce the human keratinocyte growth factor (KGF) pure proteins ...
FORESKIN KERATINOCYTE (NEONATAL) (UNII: ZJO8CP3Q2A) (FORESKIN KERATINOCYTE (NEONATAL) - UNII:ZJO8CP3Q2A) FORESKIN KERATINOCYTE ... GINTUIT- allogeneic cultured keratinocytes and fibroblasts in bovine collagen cellular sheet. Out of scope - Out of scope for ... GINTUIT- allogeneic cultured keratinocytes and fibroblasts in bovine collagen cellular sheet. To receive this label RSS feed. ... GINTUIT- allogeneic cultured keratinocytes and fibroblasts in bovine collagen cellular sheet. If this SPL contains inactivated ...
MicroRNA-223 supresses the canonical NF-kB pathway basal keratinocytes to dampen neutrophilic inflammation. Cell Reprod 13:1810 ...
Keratinocytes? Early detection/ diagnosis. Early detection is a major problem. Earlier detection more satisfactory? Visual ... markers for keratinocytes (during surgery). Surgery - type of surgery. Evidence for second looks?. Empirical, but improvements ...
TAHA, Siti Aisyah Mohd et al. Expression analysis of Notch signaling pathway molecules in SHED cultured in keratinocyte growth ... keratinocyte growth medium (KGM). Methods: RNA was extracted from SHED harvested on day 1, 3 and 7. RNA was reverse-transcribed ...
Results: PM2.5-treated keratinocytes exhibited changes in cell cycle-related genes as well as genes involved in DNA replication ... Results: PM2.5-treated keratinocytes exhibited changes in cell cycle-related genes as well as genes involved in DNA replication ... Results: PM2.5-treated keratinocytes exhibited changes in cell cycle-related genes as well as genes involved in DNA replication ... Although few studies have reported the skin diseases associated with PM2.5, its effects on keratinocytes have yet to be ...

No FAQ available that match "keratinocytes"