Bone and Bones
Bone Morphogenetic Protein 2
Bone Morphogenetic Proteins
Mesenchymal Stromal Cells
Collagen Type I
Bone Marrow Cells
Gene Expression Regulation
Reverse Transcriptase Polymerase Chain Reaction
Receptor Activator of Nuclear Factor-kappa B
Activating Transcription Factor 4
Low Density Lipoprotein Receptor-Related Protein-5
Transforming Growth Factor beta
Receptor, Parathyroid Hormone, Type 1
Wnt Signaling Pathway
Coated Materials, Biocompatible
Promoter Regions, Genetic
Intercellular Signaling Peptides and Proteins
Bone Morphogenetic Protein 6
Extracellular Matrix Proteins
Twist Transcription Factor
Bone Morphogenetic Protein 3
PHEX Phosphate Regulating Neutral Endopeptidase
Platelet-derived growth factor induces interleukin-6 transcription in osteoblasts through the activator protein-1 complex and activating transcription factor-2. (1/4631)Platelet-derived growth factor (PDGF) BB, a mitogen that stimulates bone resorption, increases the expression of interleukin-6 (IL-6), a cytokine that induces osteoclast recruitment. The mechanisms involved in IL-6 induction by PDGF BB are poorly understood. We examined the effect of PDGF BB on IL-6 expression in cultures of osteoblasts from fetal rat calvariae (Ob cells). PDGF BB increased IL-6 mRNA and heterogeneous nuclear RNA levels, the rate of transcription, and the activity of base pairs (bp) -2906 to +20 IL-6 promoter fragments transiently transfected into Ob cells. Deletion analysis revealed two responsive regions, one containing an activator protein-1 (AP-1) site located between bp -276 and -257, and a second, less well defined, downstream of -257. Targeted mutations of a cyclic AMP-responsive element (CRE), and nuclear factor-IL-6 and nuclear factor-kappaB binding sites in a bp -257 to +20 IL-6 construct that was transfected into Ob cells, revealed that the CRE also contributed to IL-6 promoter induction by PDGF BB. Electrophoretic mobility shift assay revealed AP-1 and CRE nuclear protein complexes that were enhanced by PDGF BB. Supershift assays revealed binding of Jun and Fos to AP-1 and CRE sequences and binding of activating transcription factor-2 to CRE. In conclusion, PDGF BB induces IL-6 transcription in osteoblasts by regulating nuclear proteins of the AP-1 complex and activating transcription factor-2. (+info)
Molecular cloning of mouse and bovine chondromodulin-II cDNAs and the growth-promoting actions of bovine recombinant protein. (2/4631)We previously determined the complete primary sequence of a heparin-binding growth-promoting factor, chondromodulin-II (ChM-II), which stimulated the growth of chondrocytes and osteoblasts in culture. Bovine ChM-II was a 16-kDa basic protein with 133 amino acid residues and exhibited a significant sequence similarity to the repeats of the chicken mim-1 gene product. Here we report the nucleotide sequences of bovine and mouse ChM-II cDNAs. The cDNAs each contained an open-reading frame corresponding to the ChM-II precursor with 151 amino acid residues. The N-terminus of the precursor included a secretory signal sequence of 18 amino acids prior to the mature ChM-II sequence. Unlike MIM-1, there was no repeat structure in the precursor protein, indicating that ChM-II was encoded as a gene product distinct from MIM-1. We then expressed recombinant bovine ChM-II protein which was purified to homogeneity. The recombinant protein stimulated the growth of rabbit growth plate chondrocytes, mouse MC3T3-E1 cells and rat UMR-106 osteoblastic cells in vitro. (+info)
Mechanically induced c-fos expression is mediated by cAMP in MC3T3-E1 osteoblasts. (3/4631)In serum-deprived MC3T3-E1 osteoblasts, mechanical stimulation caused by mild (287 x g) centrifugation induced a 10-fold increase in mRNA levels of the proto-oncogene, c-fos. Induction of c-fos was abolished by the cAMP-dependent protein kinase inhibitor H-89, suggesting that the transient c-fos mRNA increase is mediated by cAMP. Down-regulation of protein kinase C (PKC) activity by chronic TPA treatment failed to significantly reduce c-fos induction, suggesting that TPA-sensitive isoforms of PKC are not responsible for c-fos up-regulation. In addition, 287 x g centrifugation increased intracellular prostaglandin E2 (PGE2) levels 2.8-fold (P<0. 005). Since we have previously shown that prostaglandin E2 (PGE2) can induce c-fos expression via a cAMP-mediated mechanism, we asked whether the increase in c-fos mRNA was due to centrifugation-induced PGE2 release. Pretreatment with the cyclooxygenase inhibitors indomethacin and flurbiprofen did not hinder the early induction of c-fos by mechanical stimulation. We conclude that c-fos expression induced by mild mechanical loading is dependent primarily on cAMP, not PKC, and initial induction of c-fos is not necessarily dependent on the action of newly synthesized PGE2. (+info)
Cbfa1 isoforms exert functional differences in osteoblast differentiation. (4/4631)Cbfa1 is an essential transcription factor for osteoblast differentiation and bone formation. We investigated functional differences among three isoforms of Cbfa1: Type I (originally reported as Pebp2alphaA by Ogawa et al. (Ogawa, E., Maruyama, M., Kagoshima, H., Inuzuka, M., Lu, J., Satake, M., Shigesada, K., and Ito, Y. (1993) Proc. Natl. Acad. Sci. U. S. A. 90, 6859-6863), Type II (originally reported as til-1 by Stewart et al. (Stewart, M., Terry, A., Hu, M., O'Hara, M., Blyth, K., Baxter, E., Cameron, E., Onions, D. E., and Neil, J. C. (1997) Proc. Natl. Acad. Sci. U. S. A. 94, 8646-8651), and Type III (originally reported as Osf2/Cbfa1 by Ducy et al. (Ducy, P., Zhang, R., Geoffroy, V., Ridall, A. L., and Karsenty, G. (1997) Cell 89, 747-754). A reverse transcriptase-polymerase chain reaction analysis demonstrated that these isoforms were expressed in adult mouse bones. The transient transfection of Type I or Type II Cbfa1 in a mouse fibroblastic cell line, C3H10T1/2, induced the expression of alkaline phosphatase (ALP) activity. This induction was synergistically enhanced by the co-introduction of Xenopus BMP-4 cDNA. In contrast, the transient transfection of Type III cDNA induced no ALP activity. In C3H10T1/2 cells stably transfected with each isoform of Cbfa1, the gene expression of ALP was also strongly induced in cells transfected with Type I and Type II Cbfa1 but not in cells with Type III Cbfa1. Osteocalcin, osteopontin,and type I collagen gene expressions were induced or up-regulated in all of the cells stably transfected with each isoform of Cbfa1, and Type II transfected cells exhibited the highest expression level of osteocalcin gene. A luciferase reporter gene assay using a 6XOSE2-SV40 promoter (6 tandem binding elements for Cbfa1 ligated in front of the SV40 promoter sequence), a mouse osteocalcin promoter, and a mouse osteopontin promoter revealed the differences in the transcriptional induction of target genes by each Cbfa1 isoform with or without its beta-subunit. These results suggest that all three of the Cbfa1 isoforms used in the present study are involved in the stimulatory action of osteoblast differentiation, but they exert different functions in the process of osteoblast differentiation. (+info)
Transplantation of osteoblast-like cells to the distracted callus in rabbits. (5/4631)We carried out limb lengthening in rabbits and then transplanted osteoblast-like cells derived from the tibial periosteum to the centres of distracted callus immediately after distraction had been terminated. Two weeks later the transaxial area ratio at the centre of the distracted callus and the bone mineral density (BMD) were significantly higher in the transplanted group, by 21% and 42%, respectively, than in the non-injected group or the group injected with physiological saline (p < 0.05). Callus BMD as a percentage of density in uninvolved bone was also significantly higher in the transplanted group (p < 0.05) than in the other two groups, by 27% and 20% in the second and fourth weeks, respectively (p < 0.05). Mechanically, the callus in the transplanted group tended to be stronger as shown by the three-point bending test although the difference in fracture strength was not statistically significant. Our results show that transplantation of osteoblast-like cells promotes maturity of the distracted callus as observed at the second and fourth weeks after lengthening. The method appears promising as a means of shortening the consolidation period of callus distraction and decreasing complications during limb lengthening with an external fixator. (+info)
Leukemia inhibitory factor and oncostatin M stimulate collagenase-3 expression in osteoblasts. (6/4631)Leukemia inhibitory factor (LIF) and oncostatin M (OSM) have multiple effects on skeletal remodeling. Although these cytokines modestly regulate collagen synthesis in osteoblasts, their effects on collagenase expression and collagen degradation are not known. We tested whether LIF and OSM regulate the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in osteoblast-enriched cells isolated from fetal rat calvariae. LIF and OSM increased collagenase-3 (MMP-13) mRNA and immunoreactive protein levels in a time- and dose-dependent manner. LIF and OSM enhanced the rate of transcription of the collagenase gene and stabilized collagenase mRNA in transcriptionally arrested cells. LIF and OSM failed to regulate the expression of gelatinase A (MMP-2) and B (MMP-9). LIF and OSM modestly stimulated the expression of TIMP-1 but did not alter the expression of TIMP-2 and -3. In conclusion, LIF and OSM stimulate collagenase-3 and TIMP-1 expression in osteoblasts, and these effects may be involved in mediating the bone remodeling actions of these cytokines. (+info)
Regulation of chondrocyte differentiation by Cbfa1. (7/4631)Cbfa1, a developmentally expressed transcription factor of the runt family, was recently shown to be essential for osteoblast differentiation. We have investigated the role of Cbfa1 in endochondral bone formation using Cbfa1-deficient mice. Histology and in situ hybridization with probes for indian hedgehog (Ihh), collagen type X and osteopontin performed at E13.5, E14.5 and E17.5 demonstrated a lack of hypertrophic chondrocytes in the anlagen of the humerus and the phalanges and a delayed onset of hypertrophy in radius/ulna in Cbfa1-/- mice. Detailed analysis of Cbfa1 expression using whole mount in situ hybridization and a lacZ reporter gene reveled strong expression not only in osteoblasts but also in pre-hypertrophic and hypertrophic chondrocytes. Our studies identify Cbfa1 as a major positive regulator of chondrocyte differentiation. (+info)
A BMP-inducible gene, dlx5, regulates osteoblast differentiation and mesoderm induction. (8/4631)Bone morphogenetic proteins (BMPs), members of the transforming growth factor beta superfamily, have been identified by their ability to induce cartilage and bone from nonskeletal cells and have been shown to act as a ventral morphogen in Xenopus mesoderm. We isolated a murine homeobox-containing gene, distal-less 5 (mDlx5), as a BMP-inducible gene in osteoblastic MC3T3-E1 cells. Stable transfectants of MC3T3-E1 that overexpress mDlx5 mRNA showed increase in various osteogenic markers, a fourfold increase in alkaline phosphatase activity, a sixfold increase in osteocalcin production, and appearance in mineralization of extracellular matrix. Furthermore, mDlx5 was induced orthotopically in mouse embryos treated with BMP-4 and in fractured bone of adult mice. Consistent with these observations, we also found that injection of mDlx5 mRNA into dorsal blastomeres enhanced the ventralization of Xenopus embryos. These findings suggest that mDlx5 is a target gene of the BMP signaling pathway and acts as an important regulator of both osteogenesis and dorsoventral patterning of embryonic axis. (+info)
There are several factors that can contribute to bone resorption, including:
1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.
Bone resorption can be diagnosed through a range of tests, including:
1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.
Treatment for bone resorption depends on the underlying cause and may include:
1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.
* Osteogenesis imperfecta (OI): A genetic disorder that affects the formation of bone tissue, leading to fragile bones and an increased risk of fractures.
* Rickets: A vitamin D-deficient disease that causes softening of the bones in children.
* Osteomalacia: A condition similar to rickets, but affecting adults and caused by a deficiency of vitamin D or calcium.
* Hyperparathyroidism: A condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to an imbalance in bone metabolism and an increase in bone resorption.
* Hypoparathyroidism: A condition in which the parathyroid glands produce too little PTH, leading to low levels of calcium and vitamin D and an increased risk of osteoporosis.
Bone diseases, metabolic are typically diagnosed through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests to evaluate bone metabolism. Treatment depends on the specific underlying cause of the disease and may include medications, dietary changes, or surgery.
There are several types of osteosarcomas, including:
1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.
The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:
1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.
Symptoms of osteosarcoma may include:
1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone
If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:
1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.
There are several types of osteoporosis, including:
1. Postmenopausal osteoporosis: This type of osteoporosis is caused by hormonal changes that occur during menopause. It is the most common form of osteoporosis and affects women more than men.
2. Senile osteoporosis: This type of osteoporosis is caused by aging and is the most common form of osteoporosis in older adults.
3. Juvenile osteoporosis: This type of osteoporosis affects children and young adults and can be caused by a variety of genetic disorders or other medical conditions.
4. secondary osteoporosis: This type of osteoporosis is caused by other medical conditions, such as rheumatoid arthritis, Crohn's disease, or ulcerative colitis.
The symptoms of osteoporosis can be subtle and may not appear until a fracture has occurred. They can include:
1. Back pain or loss of height
2. A stooped posture
3. Fractures, especially in the spine, hips, or wrists
4. Loss of bone density, as determined by a bone density test
The diagnosis of osteoporosis is typically made through a combination of physical examination, medical history, and imaging tests, such as X-rays or bone density tests. Treatment for osteoporosis can include medications, such as bisphosphonates, hormone therapy, or rANK ligand inhibitors, as well as lifestyle changes, such as regular exercise and a balanced diet.
Preventing osteoporosis is important, as it can help to reduce the risk of fractures and other complications. To prevent osteoporosis, individuals can:
1. Get enough calcium and vitamin D throughout their lives
2. Exercise regularly, especially weight-bearing activities such as walking or running
3. Avoid smoking and excessive alcohol consumption
4. Maintain a healthy body weight
5. Consider taking medications to prevent osteoporosis, such as bisphosphonates, if recommended by a healthcare provider.
The disorder is characterized by a range of symptoms, including:
1. Enlarged head size and abnormal shape of the skull, which can lead to increased intracranial pressure and potentially life-threatening complications.
2. Premature fusion of certain skull sutures, resulting in a rigid and inflexible skull.
3. Abnormal development of the brain, including underdeveloped cerebral hemispheres, enlarged cerebellum, and abnormalities in the structure of the brain's corpus callosum.
4. Webbed fingers and/or toes (syndactyly), which can range from mild to severe.
5. Limb malformations, such as clubfoot or missing digits.
6. Intellectual disability, developmental delays, and/or seizures.
The exact prevalence of acrocephalosyndactylia is not known, but it is estimated to affect approximately 1 in 100,000 to 1 in 200,000 births. The disorder is usually inherited as an autosomal dominant trait, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous genetic mutations.
There is no cure for acrocephalosyndactylia, but various treatments can help manage the associated symptoms and complications. These may include surgery to relieve intracranial pressure, physical therapy to improve limb function, and medical management of seizures and other neurological issues. With appropriate support and care, individuals with acrocephalosyndactylia can lead fulfilling lives, although they may face unique challenges and limitations.
Some common types of bone diseases include:
1. Osteoporosis: A condition characterized by brittle, porous bones that are prone to fracture.
2. Osteoarthritis: A degenerative joint disease that causes pain and stiffness in the joints.
3. Rheumatoid arthritis: An autoimmune disorder that causes inflammation and pain in the joints.
4. Bone cancer: A malignant tumor that develops in the bones.
5. Paget's disease of bone: A condition characterized by abnormal bone growth and deformity.
6. Osteogenesis imperfecta: A genetic disorder that affects the formation of bone and can cause brittle bones and other skeletal deformities.
7. Fibrous dysplasia: A rare condition characterized by abnormal growth and development of bone tissue.
8. Multiple myeloma: A type of cancer that affects the plasma cells in the bone marrow.
9. Bone cysts: Fluid-filled cavities that can form in the bones and cause pain, weakness, and deformity.
10. Bone spurs: Abnormal growths of bone that can form along the edges of joints and cause pain and stiffness.
Bone diseases can be diagnosed through a variety of tests, including X-rays, CT scans, MRI scans, and bone biopsies. Treatment options vary depending on the specific disease and can include medication, surgery, or a combination of both.
Some common types of bone neoplasms include:
* Osteochondromas: These are benign tumors that grow on the surface of a bone.
* Giant cell tumors: These are benign tumors that can occur in any bone of the body.
* Chondromyxoid fibromas: These are rare, benign tumors that develop in the cartilage of a bone.
* Ewing's sarcoma: This is a malignant tumor that usually occurs in the long bones of the arms and legs.
* Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow.
Symptoms of bone neoplasms can include pain, swelling, or deformity of the affected bone, as well as weakness or fatigue. Treatment options depend on the type and location of the tumor, as well as the severity of the symptoms. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these.
Osteolysis can be caused by several factors, including:
1. Infection: Bacterial or fungal infections can cause osteolysis by secreting enzymes that break down bone tissue.
2. Inflammation: Chronic inflammation can lead to the destruction of bone tissue, causing osteolysis.
3. Tumors: Malignant tumors like multiple myeloma or osteosarcoma can cause osteolysis by producing enzymes that destroy bone tissue.
4. Degenerative conditions: Conditions like osteoporosis, rheumatoid arthritis, and Paget's disease can lead to osteolysis due to the gradual breakdown of bone tissue.
Symptoms of osteolysis may include:
1. Bone pain or tenderness
2. Fractures or fracture risk
3. Limited mobility or stiffness in affected joints
4. Swelling or redness in the affected area
5. Difficulty healing from injuries or infections
Treatment for osteolysis depends on the underlying cause and may include:
1. Antibiotics to treat infections
2. Pain management with medication or physical therapy
3. Surgery to repair or replace damaged bone tissue
4. Orthotics or assistive devices to support affected joints
5. Medications to slow down or stop bone loss, such as bisphosphonates or denosumab
In conclusion, osteolysis is a condition where there is a gradual loss or destruction of bone tissue, leading to a decrease in bone density and structural integrity. It can be caused by various factors, including infection, inflammation, tumors, and degenerative conditions. Treatment depends on the underlying cause and may include antibiotics, pain management, surgery, orthotics, and medications to slow down or stop bone loss.
There are several types of osteosclerosis, including:
1. Juvenile osteosclerosis: A rare condition that affects children and adolescents, characterized by abnormal bone growth and development.
2. Paget's disease of bone: A chronic disorder that causes enlarged and deformed bones due to excessive bone resorption and formation.
3. Osteogenesis imperfecta: A genetic disorder characterized by brittle bones, blue sclerae, and other physical abnormalities.
4. Hyperparathyroidism: A condition in which the parathyroid glands produce too much parathyroid hormone, leading to an overgrowth of bone tissue.
5. Chronic kidney disease: A condition in which the kidneys do not function properly, leading to an imbalance of minerals in the body that can cause bone abnormalities.
The symptoms of osteosclerosis can vary depending on the location and severity of the condition. Common symptoms include:
* Pain or tenderness in the affected area
* Limited mobility or stiffness in the joints
* Weakness or fatigue
* Fractures or breaks in the affected bone
* Abnormal bone growth or deformity
Treatment for osteosclerosis depends on the underlying cause of the condition. Medications such as bisphosphonates, hormone replacement therapy, or surgery may be recommended to manage symptoms and slow down the progression of the disease. In some cases, physicians may recommend lifestyle modifications such as a balanced diet, regular exercise, and avoiding substances that can harm the bones, such as tobacco and excessive alcohol consumption.
In conclusion, osteosclerosis is a condition characterized by abnormal bone growth and hardening of the bones, which can lead to a range of symptoms and complications. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help manage symptoms and prevent further damage to the bones.
The word "osteopetrosis" comes from the Greek words "osteon," meaning bone, and "petros," meaning rock or stone. This name reflects the dense and hard nature of the bones affected by the disorder.
Osteopetrosis can be caused by mutations in several genes that are involved in bone development and growth. The condition is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the disorder. However, some cases may be caused by spontaneous mutations or other factors.
Symptoms of osteopetrosis can vary depending on the severity of the disorder and the specific affected bones. Common symptoms include bone pain, limited mobility, and an increased risk of fractures. Other symptoms may include fatigue, fever, and difficulty swallowing or breathing.
Treatment for osteopetrosis usually involves a combination of medications and surgery. Medications such as bisphosphonates and denintuzumab mafodotin can help reduce bone pain and the risk of fractures, while surgery may be necessary to correct deformities or repair broken bones. In some cases, bone marrow transplantation may be recommended to replace damaged bone marrow with healthy cells.
Overall, osteopetrosis is a rare and debilitating disorder that can have a significant impact on quality of life. Early diagnosis and appropriate treatment are important for managing symptoms and preventing complications.
Osteoblast milk protein
Mir-367 microRNA precursor family
Mir-337 microRNA precursor family
Mir-32 microRNA precursor family
Mir-153 microRNA precursor family
Relative energy deficiency in sport
Osteonecrosis of the jaw
Mir-25 microRNA precursor family
Mir-423 microRNA precursor family
Vitamin B12 deficiency
Effects of TGF-β1 on OPG/RANKL Expression of Cementoblasts and Osteoblasts Are Similar without Stress but Different with...
Effect of Diosmin on Osteoblast Differentiation
Fluoride Action Network | Effects of fluoride on the proliferation and activation of osteoblasts by regulating methylation...
"P2X7 Nucleotide Receptor Signaling in Osteoblasts" by Matthew W. Grol
Genetic Portrait of Osteoblast-Like Cells Cultured on PerioGlas | Journal of Oral Implantology
The classical estrogen receptor transcriptional pathway: Implications in human osteoblasts<...
Impact of polymer-bound iodine on fibronectin adsorption and osteoblast cell morphology in radiopaque medical polymers:...
Reprogramming of Mouse Calvarial Osteoblasts into Induced Pluripotent Stem Cells. | Stem Cells Int;2018: 5280793, 2018. |...
Transcriptional control of osteoblast differentiation
Osteoblast proliferation on hydroxyapatite thin coatings produced by right angle magnetron sputtering<...
Beta1-integrin and TRPV4 are involved in osteoblast adhesion to different titanium surface topographies
Human Osteoblast - femural total RNA | ScienCell Research Laboratories
JAK/STAT guarantees robust neural stem cell differentiation by shutting off biological noise | Scientific Reports
Primary human osteoblast proliferation and prostaglandin E2 release in response to mechanical strain in vitro. - Nuffield...
Hematopoietic cell regulation of osteoblast proliferation and differentiation - Fingerprint - Augusta University Research...
Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia
FNDC5/irisin is expressed and regulated differently in human periodontal ligament cells, dental pulp stem cells and osteoblasts...
Abrogation of prostaglandin E-EP4 signaling in osteoblasts prevents the bone destruction induced by human prostate cancer...
Differentiation of MC3T3-E1 Osteoblasts is associated with temporal changes in the expression of IGF-I and IGFBPs<...
Protein Kinase A Phosphorylates Dlx3 and Regulates the Function of Dlx3 during Osteoblast Differentiation<...
Hyperphosphatemia: Practice Essentials, Background, Pathophysiology
Understanding Bone Cancer | American Cancer Society
Involvement of miR-140-3p in Wnt3a and TGFβ3 signaling pathways during osteoblast differentiation in MC3T3-E1 cells -...
The lysine methyltransferases SET and MYND domain containing 2 (Smyd2) and Enhancer of Zeste 2 (Ezh2) co-regulate osteoblast...
Hyperphosphatemia: Practice Essentials, Background, Pathophysiology
JCI - Bone marrow adipogenic lineage precursors promote osteoclastogenesis in bone remodeling and pathologic bone loss
Saladin Anatomy And Physiology Quiz - ProProfs Quiz
- The aim of this study was to examine the effects of diosmin on osteoblast differentiation using MC3T3-E1 preosteoblast cells. (fao.org)
- Diosmin regulated expression of key osteogenic genes such as dNA-binding protein inhibitor (Id1), runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteocalcin (OC) during osteoblast differentiation, and promoted recovery of tumor necrosis factor (TNF)-α-reduced osteogenesis. (fao.org)
- Diosmin enhanced mineralization and recovery of TNF-α-reduced osteoblast differentiation. (fao.org)
- These results suggest that diosmin may enhance osteoblast differentiation and recovery of TNF-α-reduced osteoblast differentiation, and it may be a candidate for treating osteoporosis. (fao.org)
- The P2X7 receptor has been shown previously to promote osteoblast differentiation, though the signaling mechanisms remain poorly defined. (uwo.ca)
- One or more of these pathways in turn may mediate the effects of P2X7 on osteoblast differentiation and mechanotransduction in bone. (uwo.ca)
- Protein kinase A (PKA), a serine/threonine kinase, regulates bone formation, and enhances Bone morphogenetic protein (BMP)-induced osteoblast differentiation. (ewha.ac.kr)
- We investigated the effects of modulating PKA activity during BMP2-induced osteoblast differentiation, and found that PKA regulates the function of Dlx3. (ewha.ac.kr)
- Dlx3 plays crucial roles in osteoblast differentiation and it is expressed in most skeletal elements during development. (ewha.ac.kr)
- These results suggest that Dlx3 is a novel target of PKA, and that PKA mediates BMP signaling during osteoblast differentiation, at least in part, by phosphorylating Dlx3 and modulating the protein stability and function of Dlx3. (ewha.ac.kr)
- The Wnt/β-catenin signaling and TGFβ signaling pathways play a key role in osteoblast differentiation. (elsevierpure.com)
- However, involvement of miRNAs is not established for Wnt3a and TGFβ signaling pathways in osteoblast differentiation. (elsevierpure.com)
- Here, we examined the role of miRNAs expressed differentially after Wnt3a expression during osteoblast differentiation. (elsevierpure.com)
- These results suggest that the miR-140-3p is involved in osteoblast differentiation as a critical regulatory factor between Wnt3a and TGFβ3 signaling pathways. (elsevierpure.com)
- Enhancer of Zeste homolog 2 (EZH2/Ezh2), a histone H3 lysine 27 (H3K27) methyl transferase, is a suppressor of osteoblast differentiation. (eur.nl)
- Here, we examined whether Smyd2 modulates Ezh2 suppression of osteoblast differentiation. (eur.nl)
- Mechanistically, Smyd2 represents a functional epigenetic regulator that operates in parallel to the suppressive effects of Ezh2 and H3K27 trimethylation on osteoblast differentiation. (eur.nl)
- We found that myocilin is expressed in bone marrow-derived mesenchymal stem cells (MSCs) and affects their differentiation into osteoblasts. (nih.gov)
- The osteogenic cell lineage MC3T3-E1, which behaves similarly to primary osteoblasts, and the cementogenic cell lineage OCCM-30, which expresses specific cementum-derived attachment protein and differentiates into terminally differentiated cementocytes, were considered good models for in vitro studies [ 4 , 5 ]. (hindawi.com)
- Herein we report the impact of increasing iodine inclusion on the cell morphology (cell area and shape) of MC3T3-E1 osteoblasts on a series of homopolymers and discrete blend thin films of poly(desaminotyrosyl tyrosine ethyl ester carbonate), poly(DTE carbonate), and an iodinated analogue poly(I(2)-DTE carbonate). (duke.edu)
- Increased PLF also promoted cell adhesion in MC3T3-E1 osteoblast-like cell cultures. (cdc.gov)
- Nucleotides are released from cells of the osteoblast lineage in response to mechanical stimulation, and signal through two families of P2 nucleotide receptors - G protein-coupled P2Y receptors and ligand-gated P2X cation channels. (uwo.ca)
- In this thesis, we demonstrate that the endogenous network of P2 receptors expressed by osteoblasts permits graded increases in Ca 2+ signaling over a million-fold range of ATP concentrations. (uwo.ca)
- These findings suggest complex transcriptional and post-transcriptional regulation of IGFBP metabolism during osteoblast development. (uky.edu)
- From a molecular point of view, it has been shown that ionic products of BG dissolution increase proliferation of human osteoblasts and induce insulin-like growth factor II messenger RNA expression and protein synthesis. (allenpress.com)
- The highest proliferation of human osteoblasts was achieved on HA RAMS-coated titanium substrates. (northwestern.edu)
- On the other hand, silencing TRPV4 strongly inhibited cell adhesion on selected substrates, proving the role of this protein in mediating osteoblasts adhesion on titanium substrates. (unito.it)
- As force-sensitive type of cells, both cementoblasts and osteoblasts change their functions and activities under mechanical stress to regulate the resorption and formation of bone and cementum [ 2 ]. (hindawi.com)
- Because the molecular events by which PG is able to alter osteoblast activity to promote bone formation are poorly understood, we investigated genes that are differently regulated in osteoblast-like cells exposed to PG. (allenpress.com)
- In previous in vitro studies on human cells, the osteoblast cell line MG63 was used as a prototype of human bone cells to test bioglass that found favorable results. (allenpress.com)
- This meeting included an overview of advances in the genomic actions of estrogen (E2) in osteoblast (OB) cells, followed by recent studies in this laboratory. (elsevier.com)
- In the wake of this demolition, bone-building cells, called osteoblasts, move in and deposit new minerals to patch and remodel the bone, maintaining its strength and durability. (nih.gov)
- Reprogramming of Mouse Calvarial Osteoblasts into Induced Pluripotent Stem Cells. (bvsalud.org)
- Following retroviral transduction of Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc), enriched population of osteoblasts underwent silencing of Osx1-GFPCre expression at early stage of reprogramming followed by late activation of Oct4-EGFP expression in the resulting iPS cells . (bvsalud.org)
- These osteoblast -derived iPS cells exhibited gene expression profiles akin to embryonic stem cells and were pluripotent as demonstrated by their ability to form teratomas comprising tissues from all germ layers and also contribute to tail tissue in chimera embryos . (bvsalud.org)
- These data demonstrate that iPS cells can be generated from intramembranous osteoblasts . (bvsalud.org)
- In vitro experiments, using murine osteoblasts, showed that cells rapidly adhere, spread and proliferate over the thin coating surface, while simultaneously generating strong in-plane stresses, as observed on SEM images. (northwestern.edu)
- Human osteoblasts were seeded at a density of 2500 cells cm -2 on silicon and titanium HA coated substrates by RAMS. (northwestern.edu)
- The aim of this study was to establish a system for applying well-defined physiological levels of mechanical strain to a well-defined population of human osteoblast-like cells. (ox.ac.uk)
- The implications of this study are that human osteoblast-like cells do respond to physiological strain in vitro, although some cells are more strain sensitive than others. (ox.ac.uk)
- By examining how mesenchymal osteolineage cells modulate haematopoiesis, here we show that deletion of Dicer1 specifically in mouse osteoprogenitors, but not in mature osteoblasts, disrupts the integrity of haematopoiesis. (nih.gov)
- However, cell-cell interactions between fixed PC-3 cells and host osteoblasts induced PGE2 production and RANKL expression in the osteoblasts. (ox.ac.uk)
- Osteoblasts are cells that lay down new bone. (cancer.org)
- Researchers believe that the RUNX2 protein acts as a "master switch," regulating a number of other genes involved in the development of cells that build bones (osteoblasts) and in the development of teeth. (medlineplus.gov)
- Research suggests that the extra genetic material in one copy of the RUNX2 gene in each cell alters the function of the RUNX2 protein, and may interfere with the maturation of cells that build bones (osteoblasts). (medlineplus.gov)
- We examined the relationship between osteoblast maturation and temporal changes in the secretion of IGF-I and the IGF-binding proteins (IGFBPs) in the MC3T3-El model of osteoblast development. (uky.edu)
- The biological response in vitro relied on β1 integrin activation that cooperated with the putative mechano-protein transient receptor potential vanilloid 4 (TRPV4) in determining the adhesion of the osteoblasts. (unito.it)
- Furthermore, the DNA methyltransferase inhibitor 5-AZA-dC suppressed cell viability , cell number in S-phase, ALP activity and osteogenesis-related protein levels in osteoblasts treated with low doses of NaF. (fluoridealert.org)
- Loss of Smyd2 protein does not affect alkaline phosphatase activity nor does it result in a unified expression response for standard osteoblast-related mRNA markers (e.g. (eur.nl)
- Addition of an EP4 antagonist suppressed both PGE2 and RANKL expression induced by the PC3-osteoblast interaction, which would have consequent effects on osteoclast activation and osteolysis. (ox.ac.uk)
- The expression levels of genes related to the function of osteoblasts, such as Runx-2 and Osteocalcin , and genes related to proliferation, such as MCM3, were remarkably increased (preliminary research on this subject). (fluoridealert.org)
- 11 In addition, a gene-expression profiling of human osteoblasts after treatment with the ionic products of BG dissolution was performed by using complementary DNA (cDNA) microarray containing 1176 genes. (allenpress.com)
- In a previous study of this subject, the osteoblasts of primary cultured mice were found to always proliferate when the fluoride dose was 5-20 mg/L, and the proliferation of osteoblasts was the highest when the fluoride dose was 10 mg/L (preliminary research on this subject). (fluoridealert.org)
- 9 Human primary osteoblasts were used to investigate the osteogenic potential of a melt-derived bioactive glass (BG). (allenpress.com)
- In primary osteoblast cultures, TNFa, MIP2 and MIP3a treatment increased PLF levels in a dose dependent manner. (cdc.gov)
- Additionally, we have found that P2X7 couples through multiple anabolic pathways in osteoblasts, including Ca 2+ /NFAT, PI3K/AKT and Wnt/β-catenin signaling. (uwo.ca)
- Meanwhile, 5-AZA-dC suppressed the increase in MGMT and MLH1 gene methylation in osteoblasts treated with low doses of NaF, leading to enhanced expression of MGMT and MLH1 mRNA. (fluoridealert.org)
- Although some studies showed that cementoblasts may differ from osteoblasts regarding responses to mechanical stresses [ 3 ], this assumption remains controversial. (hindawi.com)
- Here we adopted fluorescence-activated cell sorting -based strategy to isolate homogenous population of intramembranous calvarial osteoblasts from newborn transgenic mice carrying both Osx1-GFPCre and Oct4-EGFP transgenes . (bvsalud.org)
- NaF treatment led to methylation of the DNA repair genes MGMT and MLH1 in osteoblasts, resulting in cell proliferation and activation and causing the development of skeletal fluorosis. (fluoridealert.org)
- Previous studies have shown that the pathogenesis of skeletal fluorosis lesions is characterized mainly by aberrant proliferation and activation of osteoblasts , and the proliferation of osteoblasts is finely regulated by the cell cycle [ 3 ]. (fluoridealert.org)
- If fluoride is taken in large amounts over a long period of time, fluoride can cause abnormal proliferation and activation of osteoblasts and osteoclasts , leading to skeletal fluorosis, which can lead to pain and damage to joints and bones and even permanent disability [ 3 , 5 ]. (fluoridealert.org)
- In osteoblasts treated with NaF, excessive methylation of p16 has been reported to be induced, causing increased cell proliferation , prolonged S-phase of the cell cycle, and skeletal fluorosis progression, while the methylation inhibitor 5-aza-2-deoxycytidine (5-AZA-dC) reverses the hypermethylation of p16 induced by NaF [ 6 ]. (fluoridealert.org)
- Human Osteoblast-femural total RNA (HO-f tRNA) is prepared from early passage Human Osteoblasts-femural using the Qiagen AllPrep DNA/RNA Mini kit. (sciencellonline.com)
- Musculoskeletal RNA-seq data show that SMYD2/Smyd2 is the most highly expressed SMYD/Smyd member in human bone tissues and mouse osteoblasts. (eur.nl)
- 17. Suppression of breast cancer -associated bone loss with osteoblast proteomes via hsp90 a b1/moesin-mediated inhibition of TGFβ/FN1/CD44 signaling. (nih.gov)
- Bone formation can be attributable to ostegenesis (ie, direct stimulation of osteoblast to produce new bone), osteoconduction (which operates like a scaffold), or both processes. (allenpress.com)
- The OPG/RANKL system participates in modulation of osteoblast-mediated osteoclastogenesis influencing alveolar remodeling, as well as in root cementum resorption. (hindawi.com)
- Smyd2 loss of function analysis in mouse MC3T3 osteoblasts using siRNA depletion enhances proliferation and calcium deposition. (eur.nl)
- Cementoblasts, which mainly comprise cementum, also share many similar properties with those of osteoblasts, which are the essential components of bones. (hindawi.com)
- Effects of fluoride on the proliferation and activation of osteoblasts by regulating methylation of the DNA repair genes MGMT and MLH1. (fluoridealert.org)
- This study aimed to explore the effects of TGF- β 1 on regulating activities of cementoblasts and osteoblasts with or without stress. (hindawi.com)
- His laboratory studies the mesenchymal stem cell fate as it relates to the switch between pre-adipocytes and pre-osteoblasts. (nih.gov)
- IGF-I was present at low levels in conditioned media in proliferating preosteoblasts (3.7 ± 1.7 ng/μg DNA and 3.9 ± 0.6 at culture (days 3 and 9) and increased progressively in postmitotic differentiating osteoblasts, reaching a maximal concentration of 13.1 ± 1.5 ng/μg DNA by day 25 of culture. (uky.edu)