Transforming growth factor-beta (TGF-beta) is a potent growth regulatory protein secreted by virtually all cells in a latent form. A major mechanism of regulating TGF-beta activity occurs through factors that control the processing of the latent to t
Transforming Growth Factor beta3: A TGF-beta subtype that plays role in regulating epithelial-mesenchymal interaction during embryonic development. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta3 and TGF-beta3 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor.
Transforming growth factor-beta (TGF-beta) is a secreted polypeptide that signals via receptor serine/threonine kinases and intracellular Smad effectors. TGF-beta inhibits proliferation and induces apoptosis in various cell types, and accumulation of loss-of-function mutations in the TGF-beta receptor or Smad genes classify the pathway as a tumor suppressor in humans. In addition, various oncogenic pathways directly inactivate the TGF-beta receptor-Smad pathway, thus favoring tumor growth. On the other hand, all human tumors overproduce TGF-beta whose autocrine and paracrine actions promote tumor cell invasiveness and metastasis. Accordingly, TGF-beta induces epithelial-mesenchymal transition, a differentiation switch that is required for transitory invasiveness of carcinoma cells. Tumor-derived TGF-beta acting on stromal fibroblasts remodels the tumor matrix and induces expression of mitogenic signals towards the carcinoma cells, and upon acting on endothelial cells and pericytes, TGF-beta ...
Experimental evidence suggests that transforming growth factor (TGF) beta1 is a fibrogenic cytokine. The histopathological changes of chronic renal allograft nephropathy are dominated by fibrotic changes and TGF-beta may have an important aetiological role. This study investigated the relationship between intragraft TGF-beta gene expression and extracellular matrix protein deposition in human renal allografts ...
A TGF-beta subtype that was originally identified as a GLIOBLASTOMA-derived factor which inhibits the antigen-dependent growth of both helper and CYTOTOXIC T LYMPHOCYTES. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta2 and TGF-beta2 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor ...
|p|Noggin inhibits TGF-beta signal transduction by binding to TGF-beta family ligands and preventing them from binding to their corresponding receptors. Noggin plays a key role in neural induction by inhibiting BMP4, along with other TGF-beta signaling inhibitors such as chordin and follistatin. Mouse knockout experiments have demonstrated that noggin also plays a crucial role in bone development, joint formation, and neural tube fusion. |br/|The secreted polypeptide noggin, encoded by the NOG gene, binds and inactivates members of the transforming TGF-beta superfamily signaling proteins, such as BMP4. By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, noggin may have a principal role in creating morphogenic gradients.|/p|
Endothelial cells plated on two-dimensional (2-D) substrata proliferate until they form a tightly apposed confluent monolayer of quiescent cells that display a typical cobblestone morphology. When added to proliferating cultures TGF beta-1 (transforming growth factor beta-1) inhibited cell growth and caused marked morphological changes, with the cells becoming enlarged and ragged. These effects were dose-dependent and reversible. TGF beta-1 also reduced the cloning efficiency and colony size of these cells, indicating that TGF beta-1 is cytotoxic and cytostatic for endothelial cells. By contrast, TGF beta-1 added to quiescent cobblestone cultures did not affect cell morphology or cell numbers. In the presence of 20% serum, the level of total protein synthesis per cell was significantly increased by TGF beta-1 in a dose-dependent manner when the cells were cultured on a 2-D substratum, regardless of whether the cells were proliferating or cobblestone quiescent. The level of plasminogen ...
Isoform-specific antibodies to TGF beta 1, TGF beta 2, and TGF beta 3 proteins were generated and have been used to examine the expression of these factors in the developing mouse embryo from 12.5-18.5 d post coitum (d.p.c.). These studies demonstrate the initial characterization of both TGF beta 2 and beta 3 in mammalian embryogenesis and are compared with TGF beta 1. Expression of one or all three TGF beta proteins was observed in many tissues, e.g., cartilage, bone, teeth, muscle, heart, blood vessels, lung, kidney, gut, liver, eye, ear, skin, and nervous tissue. Furthermore, all three TGF beta proteins demonstrated discrete cell-specific patterns of expression at various stages of development and the wide variety of tissues expressing TGF beta proteins represent all three primary embryonic germ layers. For example, specific localization of TGF beta 1 was observed in the lens fibers of the eye (ectoderm), TGF beta 2 in the cortex of the adrenal gland (mesoderm), and TGF beta 3 in the cochlear ...
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RUNX3 inhibits cell proliferation and induces apoptosis by reinstating transforming growth factor beta responsiveness in esophageal adenocarcinoma cells.
Artur » Lista över publikationer » ENHANCED JUN GENE-EXPRESSION IS AN EARLY GENOMIC RESPONSE TO TRANSFORMING GROWTH FACTOR BETA STIMULATION ...
In the present study, concentrations of TGF-β1 in plasma were decreased in 87% of patients with Guillain-Barré syndrome on admission, increased with motor function up to control concentrations during the next 15 days at the time of early recovery, and correlated well with the disability score. TNF-α concentrations were raised in 60% of patients on admission, and did not significantly decrease from day 1 to day 15 of the hospital stay. Other cytokines were either randomly increased (IL-2, IL-6), or undetectable in the circulation (IL-1, IL-4, IL-7, IL-10).. Treatments could not account for the down regulation of TGF-β1 seen on admission of patients. During treatment, both patients undergoing PE and patients receiving IVIg had decreased plasma concentrations of TGF-β1. PE was associated with lower concentrations of TGF-β1 in plasma than IVIg at day 7. This could have resulted from some removal of TGF-β1 (PE), or addition of TGF-β1 (IVIg) at the time of treatment.. Direct down regulation of ...
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TGFBR1 are transmembrane tyrosine kinases or associated with cytoplasmic tyrosine kinase TGF-βs » specificity with type II receptors activating type I receptors, has the pre-helix extension and its role in binding are present on the plasma membrane (cytoplasmic domain) both as monomers and homo- and hetero-oligomers chromosome 9q22.33. 6 : [§§; †, ‡]. Activin receptor-like…
rat Madh4 protein: DPC4 - Deleted in Pancreatic Carcinoma 4; inactivation may lead to pancreatic cancer; Smad family of gene products are involved in TGF-beta signal transduction pathway; RefSeq NM_019275
View mouse Tgfb1i1 Chr7:128246812-128255699 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
TGF-β and its related factors regulate a broad range of cellular functions, including proliferation, differentiation, apoptosis, migration, and adhesion. These factors are also very important in the pathogenesis of cancer and many other diseases. Although much has been known about the TGF-β signaling pathway since the discovery of Smads 15 years ago, remarkable progress has been made in revealing details of different regulatory mechanisms that afford a full range of control of the biological functions of these factors in the TGF-β family. Specific physiological and pathological roles of TGF-β/Smad in different cellular context also start to emerge. This collection of review articles provides a broad, albeit not all-inclusive, overview of the latest breakthroughs and developments in TGF-β signaling and biology. Dr Ying Zhang. ...
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Zwijsen A., Goumans M.J., Lawson K.A., Van Rooijen M.A., Mummery C.L.. Transforming growth factor beta (TGFbeta) regulates the cell cycle and extracellular matrix (ECM) deposition of many cells in vitro. We have analysed chimaeric mouse embryos generated from embryonic stem cells with abnormal receptor expression to study the effect of TGFbeta on these processes in vivo and the consequences for normal development. The binding receptor for TGFbeta, TbetaRII, is first detected in the embryo proper around day 8.5 in the heart. Ectopic expression of TbetaRII from the blastocyst stage onward resulted in an embryonic lethal around 9.5 dpc. Analysis of earlier stages revealed that the primitive streak of TbetaRII chimaeras failed to elongate. Furthermore, although cells passed through the streak and initially formed mesoderm, they tended to accumulate within the streak. These defects temporally and spatially paralleled the expression of the TGFbeta type I receptor, which is first expressed in the node ...
TGF-β1, human recombinant protein (E. Coli) , Transforming growth factor beta-1, TGF-beta-1, CED, DPD1, TGFB, TGF-b 1, LAP, TGFB1. validated in (PBV11402r-10), Abgent
The role of transforming growth factors type beta (TGF-beta) was investigated during murine embryogenesis. There are three known mammalian TGF-beta genes. The developmental pattern of expression of TGF-beta RNA has previously been elucidated by in situ hybridisation and the localisation of TGF-beta1 protein by immunohistochemistry. Based on this data it has been suggested that TGF-beta1 acts in both a paracrine and autocrine role during development. The expression of both TGF-beta2 and TGF-beta3 RNA has been observed in murine embryos by Northern analysis. In order to understand the role of these two genes, individually, and in relation with each other, the developmental regulation of all three genes was investigated by in situ hybridisation using mouse specific probes on serial mouse embryo sections from 6.5 days p.c. to 16.5 days p.c.. A comparison was made of the data concerning the temporal and spatial expression patterns of TGF-beta1, TGF-beta2 and TGF-beta3 RNA, and the role of each gene ...
Transforming growth factor-beta receptor III (TGF-beta RIII) is one of three receptors for the secreted growth factor TGF-beta. Unlike type I and type II TGF-beta receptors, TGF-beta RIII does not participate directly in the propagation of intracellular signaling in response to TGF-beta binding.
To better define the role of Ids in melanomagenesis, we hypothesized expressing Id2, Id3 or Id4 along with Smad7 would revert 1205Lu/S7 cells back to the tumorigenic state. Subcutaneous injection of TGF-β-dependent 1205Lu cells co-expressing Id2, Id3, or Id4, with Smad7 bypassed the tumorigenic block mediated by Smad7, generating TGF-β-independent tumors and re-upregulated metastasis-related genes. Surprisingly, 1205Lu/S7 cells expressing Id4, but not Id2 or Id3, activated robust melanin production in amelanotic 1205Lu cells, confirmed by Fontana-Masson stain, de-novo expression of MART-1 and tyrosinase proteins. Mechanistic investigation revealed M-MITF phosphorylation and MART-1 promoter activation in 1205Lu and WM852 melanoma cells, suggesting broader implications for Id4 in melanoma. In human tumors melanin corresponded with Id4 localization. Additionally, pigment-laden CD163+ mouse histiocytes, with areas of extensive necrosis were found throughout S7/Id4 tumors only. Current ...
Members of the transforming growth factor beta (TGF beta) family initiate cellular responses by binding to TGF beta receptor type II (Tf3R11) and type I (TpRI) serine/threonine kinases, whereby Srnad2 and Smad3 are phosphorylated and activated, promoting their association with Smadzi. We report here that T beta RI interacts with the SH3 domains of the adaptor protein CIN85 in response to TGF beta stimulation in a TRAF6-dependent manner. Small interfering RNA mediated knockdown of CIN85 resulted in accumulation of T beta RI in intracellular compartments and diminished TGF beta-stimulated Sniad2 phosphorylation. Overexpression of CIN85 instead increased the amount of T beta RI at the cell surface. This effect was inhibited by a dominant-negative mutant of Rab11, suggesting that CIN85 promoted recycling of TGF beta receptors. CIN85 enhanced TGF beta-stimulated Smad2 phosphorylation, transcriptional responses, and cell migration. CIN85 expression correlated with the degree of malignancy of prostate ...
Clone CH6-17E5.1 reacts with the N-terminal latency-associated peptide (LAP) of the transforming growth factor β1 (TGF-β1) dimer. TGF-β1 belongs to a family of homologous, disulfide-linked, homodimeric proteins. These highly pleiotropic cytokines inhibit proliferation of most cells, but can promote the growth of mesenchymal cells and enhance extracellular matrix formation. The pivotal function of TGF-β1 in the immune system is to mediate immunosuppression and maintain tolerance by regulating lymphocyte proliferation, differentiation, and survival. TGF-β1 is produced by many cell types, but is reported to be most abundant in mammalian platelets and bone. It is secreted predominantly as an inactive latent complex. After proteolytical processing of the TGF-β1 precursor, the resulting N-terminal latency-associated peptide (LAP) remains non-covalently associated with the TGF-β1 dimer. Mature and biologically active TGF-β1 can be released from the complex by action of proteases and/or conformational
TY - JOUR. T1 - Decreased transforming growth factor beta1 in autism. T2 - A potential link between immune dysregulation and impairment in clinical behavioral outcomes. AU - Ashwood, Paul. AU - Enstrom, Amanda. AU - Krakowiak, Paula. AU - Hertz-Picciotto, Irva. AU - Hansen, Robin L. AU - Croen, Lisa A.. AU - Ozonoff, Sally J. AU - Pessah, Isaac N. AU - Van de Water, Judith A. PY - 2008/11/15. Y1 - 2008/11/15. N2 - Autism spectrum disorders (ASD) are characterized by impairment in social interactions, communication deficits, and restricted repetitive interests and behaviors. There is evidence of both immune dysregulation and autoimmune phenomena in autism. We examined the regulatory cytokine transforming growth factor beta-1 (TGFβ1) because of its role in controlling immune responses. Plasma levels of active TGFβ1 were evaluated in 75 children with ASD compared with 68 controls. Children with ASD had significantly lower plasma TGFβ1 levels compared with typically developing controls (p = ...
Previous studies have indicated that the cytokine transforming growth factor beta 1 (TGF beta 1) has immunosuppressive properties and can inhibit the production of tumor necrosis factor (TNF) and Interleukin 1 (IL 1) by human peripheral blood mononuclear cells. In this study, we have examined the effects of TGF beta 1 on the production of Interleukin 6 (IL 6) by human peripheral blood mononuclear cells. Treatment with only TGF beta 1 leads to the induction of IL 6, and this was both dose- and time-dependent. The effect of TGF beta 1 was evident at the level of IL 6 mRNA, suggesting TGF beta 1-induced de novo synthesis of IL 6. Induction of IL 6 by TGF beta 1 was specific, as other cytokines made by mononuclear cells (TNF and IL 1) were not induced by TGF beta 1. Furthermore, when a panel of stimuli were compared for their ability to induce IL 1, TNF and IL 6 in the presence or absence of TGF beta 1, IL 6 levels were augmented in the presence of TGF beta 1, while the induction of IL 1 and TNF was
Transforming growth factor beta (TGF-β) is a multifunctional cytokine belonging to the transforming growth factor superfamily that includes four different isoforms (TGF-β 1 to 4, HGNC symbols TGFB1, TGFB2, TGFB3, TGFB4) and many other signaling proteins produced by all white blood cell lineages. Activated TGF-β complexes with other factors to form a serine/threonine kinase complex that binds to TGF-β receptors, which is composed of both type 1 and type 2 receptor subunits. After the binding of TGF-β, the type 2 receptor kinase phosphorylates and activates the type 1 receptor kinase that activates a signaling cascade. This leads to the activation of different downstream substrates and regulatory proteins, inducing transcription of different target genes that function in differentiation, chemotaxis, proliferation, and activation of many immune cells. TGF-β is secreted by many cell types, including macrophages, in a latent form in which it is complexed with two other polypeptides, latent ...
Serine protease with a variety of targets, including extracellular matrix proteins such as fibronectin. HTRA1-generated fibronectin fragments further induce synovial cells to up-regulate MMP1 and MMP3 production. May also degrade proteoglycans, such as aggrecan, decorin and fibromodulin. Through cleavage of proteoglycans, may release soluble FGF-glycosaminoglycan complexes that promote the range and intensity of FGF signals in the extracellular space. Regulates the availability of insulin-like growth factors (IGFs) by cleaving IGF-binding proteins. Inhibits signaling mediated by TGF-beta family members. This activity requires the integrity of the catalytic site, although it is unclear whether TGF-beta proteins are themselves degraded. By acting on TGF-beta signaling, may regulate many physiological processes, including retinal angiogenesis and neuronal survival and maturation during development. Intracellularly, degrades TSC2, leading to the activation of TSC2 downstream targets ...
TGF-beta is a secreted cytokine, which plays an important role in cell development, differentiation, and homeostasis in both physiologic and pathologic conditions, such as tumorigenesis, abnormal wound healing and skin cancer. TGF-beta transmit signal from the extracellular environment to intracellular signaling networks via its cell surface receptor complex, the TGF-beta type II/ I receptor (TbetaRII/TbetaRI) heterodimer. TGF-beta ligand binds to TbetaRII, which in turn recruits and activates TbetaRI, resulting in activation of downstream signaling complex, receptor Smads (R-Smads) and common Smad4. TGF-beta stimulation is also known to activate R-Smad-independent signaling pathways, such as the extracellular signal-regulated kinase (ERK1/2) pathway. However, two long-standing questions remained: 1) why TGF-beta activates ERK depends on the cell context and 2) whether or not TbetaRII is able to mediate the TGF-beta signaling without the participation of TbetaRI. In the chapter two, it is shown ...
Transforming growth factor beta 1 or TGF-β1 is a polypeptide member of the transforming growth factor beta superfamily of cytokines. It is a secreted protein that performs many cellular functions, including the control of cell growth, cell proliferation, cell differentiation and apoptosis. In humans, TGF-β1 is encoded by the TGFB1 gene. TGF-β is a multifunctional set of peptides that controls proliferation, differentiation, and other functions in many cell types. TGF-β acts synergistically with TGFA in inducing transformation. It also acts as a negative autocrine growth factor. Dysregulation of TGF-β activation and signaling may result in apoptosis. Many cells synthesize TGF-β and almost all of them have specific receptors for this peptide. TGF-β1, TGF-β2, and TGF-β3 all function through the same receptor signaling systems. TGF-β1 was first identified in human platelets as a protein with a molecular mass of 25 kilodaltons with a potential role in wound healing. It was later ...
Cytokines of the transforming growth factor beta (TGF-beta) superfamily, including TGF-betas, activins and bone morphogenetic proteins (BMPs), bind to specific serine/threonine kinase receptors and transmit intracellular signals through Smad proteins. Upon ligand stimulation, Smads move into the nucleus and function as components of transcription complexes. TGF-beta and BMP signaling is regulated positively and negatively through various mechanisms. Positive regulation amplifies signals to a level sufficient for biological activity. Negative regulation occurs at the extracellular, membrane, cytoplasmic and nuclear levels. TGF-beta and BMP signaling is often regulated through negative feedback mechanisms, which limit the magnitude of signals and terminate signaling. Negative regulation is also important for formation of gradients of morphogens, which is crucial in developmental processes. In addition, other signaling pathways regulate TGF-beta and BMP signaling through cross-talk. Nearly 20 BMP ...
The transforming growth factor‐β (TGF‐β) superfamily constitutes a large family of secreted signaling molecules which are known to have important roles in regulating a wide variety of cellular processes including proliferation, differentiation, adhesion and migration (Roberts and Sporn, 1990; Kingsley, 1994). All known receptors of this superfamily signal through a heteromeric complex of type I and type II transmembrane receptor serine/threonine kinases which act in series (Derynck and Feng, 1997; Massague, 1998). Despite extensive knowledge about the receptor activation mechanisms, which involve recruitment and activation of the type I receptor kinase by the ligand‐activated type II receptor kinase, the downstream signaling pathways from the activated type I receptor are not yet clearly defined. Recently, a set of novel mammalian proteins, termed SMADs, has been identified based on their high homology to the Drosophila Mad and the Caenorhabditis elegans Sma proteins, which were ...
TY - JOUR. T1 - Transforming growth factor-beta protection of cancer cells against tumor necrosis factor cytotoxicity is counteracted by hyaluronidase (review).. AU - Chang, N. S.. PY - 1998/12. Y1 - 1998/12. N2 - Numerous cancer cells, when exposed to transforming growth factor beta (TGF-beta), become resistant to tumor necrosis factor (TNF) cytotoxicity. Pretreatment of L929 fibroblasts, for example, with TGF-beta isoforms (beta 1, beta 2 and beta 3) for at least 0.5-1 h results in resistance to TNF killing. TGF-beta 1 mediates the following sequential events in L929 cells: i) rapid induction of protein tyrosine-phosphorylation (, 30 min), ii) stimulation of protective protein synthesis and acquisition of TNF resistance (approximately 0.5-1 h), and iii) suppression of I kappa B-alpha expression (1-2 h). Two protective proteins induced by TGF-beta 1 are a 46 kDa extracellular matrix TNF-resistance triggering (TRT) protein and a putative transmembrane anti-apoptotic adhesion protein TIF2 ...
Transforming growth factor beta (TGF-beta) has a strong impact on liver development and physiopathology, exercised through its pleiotropic effects on growth, differentiation, survival, and migration. When exposed to TGF-beta, the mhAT3F cells, immortalized, highly differentiated hepatocytes, maintained their epithelial morphology and underwent dramatic alterations of adhesion, leading to partial or complete detachment from a culture plate, followed by readhesion and spreading. These alterations of adhesive behavior were caused by sequential changes in expression of the alpha5beta1 integrin and of its ligand, the fibronectin. The altered specificity of anchorage to the extracellular matrix gave rise to changes in cells collective motility: cohorts adhering to fibronectin maintained a persistent, directional motility, with ezrin-rich pathfinder cells protruding from the tips of the cohorts. The absence of adhesion to fibronectin prevented the appearance of polarized pathfinders and lead to ...
Koeck, E.S., Iordanskaia, T., Sevilla, S., Ferrante, S.C., Hubal, M.J. et al. (2014). Adipocyte exosomes induce transforming growth factor beta pathway dysregulation in hepatocytes: A novel paradigm for obesity-related liver disease. Journal of Surgical Research, 192(2), 268-275.. ...
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Follicle-restricted compartmentalization of transforming growth factor beta superfamily ligands in the feline ovary.. Biol Reprod. 2004 Mar;70(3):846-59. Authors: Bristol SK, Woodruff TK ...
Transforming growth factor β1 (TGF-β1) belongs to a family of homologous, disulfide-linked, homodimeric proteins. These highly pleiotropic cytokines inhibit proliferation of most cells, but can promote the growth of mesenchymal cells and enhance extracellular matrix formation. The pivotal function of TGF-β1 in the immune system is to mediate immunosuppression and maintain tolerance by regulating lymphocyte proliferation, differentiation, and survival. - Österreich
Scientists have long known that a small protein Dr. Saikumar was studying, Transforming Growth Factor-Beta (TGF-B), behaves in a paradoxical way. When a cell begins undergoing the transformation into a cancerous state, TGF-B can stop that growth and protects us from developing cancer. But if that cell escapes the TGF-B surveillance, then it will advance into a full-blown cancer cell and TGF-B can help it thrive and spread faster.. "Turning off this treasonous action of TGF-B alone may indeed be advantageous," the pathologist said.. Although TGF-B has received intense scrutiny in the 30 years since its discovery, little is understood as to just how it turns from a tumor suppressor into a tumor promoter. Researchers found that if they suppress TGF-B activity to starve a cancerous tumor, a new tumor is likely to start growing, since the proteins helpful function in preventing new cancerous development is also switched off.. But Dr. Saikumar found a clue in an obscure protein called TMEPAI, and ...
|p|SD-208 Description:|br /|EC50: SD-208 inhibits the growth inhibition of TGF-β–sensitive CCL64 cells at an EC50 of 0.1 μmol/L .|br /|The cytokine transforming growth factor (TGF)-β has become a major target for the experimental treatm
Complete information for TGFB3 gene (Protein Coding), Transforming Growth Factor Beta 3, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
111713 - Comparación de la concentración de factores de crecimiento transformante beta I, mediante 2 métodos de obtención de sangre en perros clínicamente sanos - Comparison of the concentration of transforming growth factors beta I by 2 methods of | Veterinaria.org . La primera comunidad veterinaria de habla hispana con presencia en Espa a y Am rica del Sur.
|p|Transforming growth factor (TGF)-β signaling facilitates tumor growth and metastasis in advanced cancer. Use of inhibitors of TGF-β signaling may thus be a novel strategy for the treatment of patients with such cancer. A-77-01 is a close anal
Transforming growth factor-β (TGF-β) plays a significant role in tumour progression and metastasis, most likely through induction of immunosuppression in the
MDCK cells constitutively secrete endogenous TGF-β1 but only activate it under subconfluent conditions. (A) Latent TGF-β1 is activated only in subconfluent ce
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The production and growth regulatory activity of transforming growth factor beta were studied in human thyroid tissue. As estimated by its mRNA expression in fresh tissue samples, transforming growth factor beta was produced in normal and in diseased thyroid glands. Transforming growth factor beta mRNA was mainly produced by thyroid follicular cells and in lesser quantities by thyroid infiltrating mononuclear cells. The concentrations of transforming growth factor beta mRNA were lower in iodine-deficient nontoxic goiter than in Graves disease and normal thyroid tissue. Transforming growth factor beta protein secretion by cultured thyroid follicular cells was also low in nontoxic goiter, but could be increased by addition of sodium iodide (10 microM) to the culture medium. Recombinant transforming growth factor beta did not affect basal tritiated thymidine incorporation in cultured thyroid follicular cells, but inhibited, at a concentration of 10 ng/ml, the growth stimulatory influence of insulin-like