Transforming growth factor 3 (TGF-3) induces leukocyte recruitment and activation, events central to an inflammatory response. In this study, we demonstrate that antagonism of TGF-3 with a neutralizing antibody not only blocks inflammatory cell accumulation, but also tissue pathology in an experimental model of chronic erosive polyarthritis. Intraarticular injection of monoclonal antibody 1Dll....

Skin fibroblasts from two cases of autosomal recessive cutis laxa (CL), having insignificant elastin production and mRNA levels, were challenged with transforming growth factor beta-i (TGF-fi1). Elastin production was brought from undetectable values to amounts typical of normal human skin fibroblasts in a dose-dependent fashion. Basic fibroblast growth factor (100 ng/ml) alone or in combinatio...

Transcriptional repression of the transforming growth factor (TGF)-b type II receptor (TbRII) gene appears to be a major mechanism to inactivate TGF-b responsiveness in many human cancers. Because histone acetylation/deacetylation plays a role in transcriptional regulation, we have examined the effect of MS-275, a synthetic inhibitor of histone deacetylase, in human breast cancer cell lines. MS...

Objective: Intracellular signaling of activin and transforming growth factor-b (TGF-b) is thought to be mediated by the same molecules (Smad2/3 and Smad4). Although differentiation of murine erythroleukemia F5-5.fl cells is induced by activin, it is not induced by TGF-b, suggesting that at some point TGF-b signaling is defective. The aim of this study was to investigate the unresponsiveness of ...

In breast and colon cancers, transforming growth factor (TGF)-B signaling initially has an antineoplastic effect, inhibiting tumor growth, but eventually exerts a proneoplastic effect, increasing motility and cancer spread. In prostate cancer, studies using human samples have correlated the loss of the TGF-B type II receptor (TBRII) with higher tumor grade. To determine the effect of an inhibit...

Transforming growth factor-b (TGF-b) is known to regulate chondrocyte proliferation and hypertrophic differentiation in embryonic bone cultures by a perichondrium dependent mechanism. To begin to determine which factors in the perichondrium mediate the effects of TGF-b, we studied the effect of Insulin-like Growth Factor-1 (IGF-I) and Fibroblast Growth Factors-2 and -18 (FGF2, FGF18) on metatar...

lar pathological finding in renal diseases, and it is observed in most proliferative nephritises (including immunoglobulin A (IgA) nephropathy). The mechanism of action of the expansion of the glomerular mesangial region, a particularly notable feature of IgA nephropathy, is not well elucidated, but it is presumed that the inflammatory reactions after deposition of IgA play a critical role. Spo...

The TGF-b, a tumor suppressive cytokine in normal cells, is abused in cancer to promote the malignancy. In this study, we reported that TGF-b downregulated the mutS homolog 2 (MSH2), a central component of the DNA mismatch repair (MMR) system, in HER2-transformed MCF10A mammary epithelial cells and in breast cancer (BC) cells. This was mediated by a TGF-b–induced micro RNA (miRNA), miR-21, whic...

This study determined the contribution of extracellular matrix (ECM) remodeling to the protective adaptation of human skeletal muscle known as the repeated-bout effect (RBE). Muscle biopsies were obtained 3 hours, 2 days, and 27 days following an initial bout (B1) of lengthening contractions (LCs) and 2 days following a repeated bout (B2) in 2 separate studies. Biopsies from the nonexercised le...