The Experts below are selected from a list of 2265 Experts worldwide ranked by ideXlab platform

Kathleen M. Mulder - One of the best experts on this subject based on the ideXlab platform.

  • Transforming growth factor-β signal transduction in epithelial cells
    Pharmacology & therapeutics, 2001
    Co-Authors: Jianbo Yue, Kathleen M. Mulder
    Abstract:

    Transforming growth factor (TGF)-beta is a natural and potent growth inhibitor of a variety of cell types, including epithelial, endothelial, and hematopoietic cells. The ability of TGF-beta to potently inhibit the growth of many solid tumors of epithelial origin, including breast and colon carcinomas, is of particular interest. However, many solid tumor cells become refractory to the growth inhibitory effects of TGF-beta due to defects in TGF-beta signaling pathways. In addition, TGF-beta may stimulate the invasiveness of tumor cells via the paracrine effects of TGF-beta. Accordingly, in order to develop more effective anticancer therapeutics, it is necessary to determine the TGF-beta signal transduction pathways underlying the growth inhibitory effects and other cellular effects of TGF-beta in normal epithelial cells. Thus far, two primary signaling cascades downstream of the TGF-beta receptors have been elucidated, the Sma and Mothers against Decapentaplegic homologues and the Ras/mitogen-activated protein kinase pathways. The major objective of this review is to summarize TGF-beta signaling in epithelial cells, focusing on recent advances involving the Sma and Mothers against Decapentaplegic homologues and Ras/mitogen-activated protein kinase pathways. This review is particularly timely in that it provides a comprehensive summary of both signal transduction mechanisms and the cell cycle effects of TGF-beta.

Sun Gui-fan - One of the best experts on this subject based on the ideXlab platform.

  • Review on the role of TGF-β1/Smads signaling in the formation of hypertrophic scar
    Journal of Traumatic Surgery, 2015
    Co-Authors: Sun Gui-fan
    Abstract:

    Hypertrophic scars( HS) form as a result of pathological wound healing. By causing pain,pruritus and contractures,HS significantly affects the patients' quality of life,both physically and psychologically. Overproliferation of myofibroblasts and excessive deposition of extracellular matrix are characteristics of the HS,which are dominantly regulated by transforming growth factor-β1/drosophila Mothers against Decapentaplegic proteins( TGF-β1 /Smads) signaling. By inhibiting the signaling of TGF-β1 /Smads,HS can be alleviated. Multiple researches focus on preventing or attenuating HS against the signaling,providing important basis for therapies of HS. In this paper we summarize the roles of myofibroblasts and extracellular matrix in the process of HS,and the regulation of TGF-β1/Smads signaling during HS formation.

Jianbo Yue - One of the best experts on this subject based on the ideXlab platform.

  • Transforming growth factor-β signal transduction in epithelial cells
    Pharmacology & therapeutics, 2001
    Co-Authors: Jianbo Yue, Kathleen M. Mulder
    Abstract:

    Transforming growth factor (TGF)-beta is a natural and potent growth inhibitor of a variety of cell types, including epithelial, endothelial, and hematopoietic cells. The ability of TGF-beta to potently inhibit the growth of many solid tumors of epithelial origin, including breast and colon carcinomas, is of particular interest. However, many solid tumor cells become refractory to the growth inhibitory effects of TGF-beta due to defects in TGF-beta signaling pathways. In addition, TGF-beta may stimulate the invasiveness of tumor cells via the paracrine effects of TGF-beta. Accordingly, in order to develop more effective anticancer therapeutics, it is necessary to determine the TGF-beta signal transduction pathways underlying the growth inhibitory effects and other cellular effects of TGF-beta in normal epithelial cells. Thus far, two primary signaling cascades downstream of the TGF-beta receptors have been elucidated, the Sma and Mothers against Decapentaplegic homologues and the Ras/mitogen-activated protein kinase pathways. The major objective of this review is to summarize TGF-beta signaling in epithelial cells, focusing on recent advances involving the Sma and Mothers against Decapentaplegic homologues and Ras/mitogen-activated protein kinase pathways. This review is particularly timely in that it provides a comprehensive summary of both signal transduction mechanisms and the cell cycle effects of TGF-beta.

Peter Ten Dijke - One of the best experts on this subject based on the ideXlab platform.

  • identification of smad2 a human mad related protein in the transforming growth factor β signaling pathway
    Journal of Biological Chemistry, 1997
    Co-Authors: Atsuhito Nakao, Eva Roijer, Takeshi Imamura, Serhiy Souchelnytskyi, Goran Stenman, Carlhenrik Heldin, Peter Ten Dijke
    Abstract:

    Abstract Transforming growth factor-β (TGF-β) superfamily members are multifunctional cytokines that exert their effects via heteromeric complexes of two distinct serine and threonine kinase receptors. Drosophila Mothers against Decapentaplegic and related genes in Caenorhabditis elegans, Xenopus, and mammals were shown to function downstream in the intracellular signaling pathways of TGF-β superfamily members. Here we report the cloning of a Mad-related protein, termed Sma- and Mad-related protein 2 (Smad2). TGF-β stimulated the phosphorylation and nuclear translocation of Smad2 in nontransfected Mv1Lu cells. In addition, we demonstrated that TGF-β and activin mediated phosphorylation of Smad2 after its overexpression with appropriate type I and II receptors in COS cells. Smad2 and Smad1 were found to be broadly expressed in human tissues. Smad2 is closely linked to DPC4 on chromosome 18q21.1, a region often deleted in human cancers. Cells that lack Smad2 may escape from TGF-β-mediated growth inhibition and promote cancer progression.

Masakazu Takayasu - One of the best experts on this subject based on the ideXlab platform.

  • Eotaxin-3 activates the Smad pathway through the transforming growth factor beta 1 in chronic subdural hematoma outer membranes.
    Journal of neurotrauma, 2014
    Co-Authors: Koji Osuka, Yasuo Watanabe, Nobuteru Usuda, Masahiro Aoyama, Mikinobu Takeuchi, Masakazu Takayasu
    Abstract:

    Abstract Chronic subdural hematoma (CSDH) is considered to be an inflammatory disease. Eosinophils are frequently expressed in the outer membrane of CSDH and are major sources of transforming growth factor beta (TGF-β). The Mothers against Decapentaplegic (Smad)-signaling pathway, which is activated by TGF-β, has been shown to be involved with fibrosis. In the present study, we compared the concentrations of eotaxin-3, eosinophil-specific chemoattractant, and TGF-β between CSDH fluid and cerebrospinal fluid (CSF) from control patients. We also explored the expression of the Smad-signaling pathway in the outer membrane of CSDH. Eight patients whose outer membrane and 12 whose CSDH fluid were successfully obtained during trepanation surgery were included in the study. Concentrations of eotaxin-3 and TGF-β were measured by enzyme immunoassay kits. Expression levels of Smad2, phosphorylated Smad3, Smad3, Smad4, and actin were examined by Western blot analysis. In addition, expression of Smad3 was also examine...