NDLI: Transforming growth factor-ß (TGF-ß)-mediated connective tissue growth factor (CTGF) expression in hepatic stellate cells requires Stat3 signaling activation.

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Transforming growth factor-ß (TGF-ß)-mediated connective tissue growth factor (CTGF) expression in hepatic stellate cells requires Stat3 signaling activation.

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Transforming growth factor-ß (TGF-ß)-mediated connective tissue growth factor (CTGF) expression in hepatic stellate cells requires Stat3 signaling activation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Liu, Yan Li, Jun Weng, Honglei Dooley, Steven Nadalin, Silvio Meyer, Christoph Ten Dijke, Peter Königsrainer, Alfred Liu, Heng
Description	Author Affiliation: Liu Y ( From the Department of Medicine II, Section Molecular Hepatology, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany.)
Abstract	In fibrotic liver, connective tissue growth factor (CTGF) is constantly expressed in activated hepatic stellate cells (HSCs) and acts downstream of TGF-ß to modulate extracellular matrix production. Distinct from other cell types in which Smad signaling plays major role in regulating CTGF production, TGF-ß stimulated CTGF expression in activated HSCs is only in part dependent on Smad3. Other signaling molecules like MAPKs and PI3Ks may also participate in this process, and the underlying mechanisms have yet to be clarified. In this study, we report involvement of Stat3 activation in modulating CTGF production upon TGF-ß challenge in activated HSCs. Stat3 is phosphorylated via JAK1 and acts as a critical ALK5 (activin receptor-like kinase 5) downstream signaling molecule to mediate CTGF expression. This process requires de novo gene transcription and is additionally modulated by MEK1/2, JNK, and PI3K pathways. Cell-specific knockdown of Smad3 partially decreases CTGF production, whereas it has no significant influence on Stat3 activation. The total CTGF production induced by TGF-ß in activated HSCs is therefore, to a large extent, dependent on the balance and integration of the canonical Smad3 and Stat3 signaling pathways.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	42
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-10-18
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Connective Tissue Growth Factor Biosynthesis Gene Expression Regulation Hepatic Stellate Cells Metabolism Liver Cirrhosis MAP Kinase Signaling System STAT3 Transcription Factor Transforming Growth Factor Beta Cell Line, Transformed Genetics Extracellular Matrix Physiology Extracellular Signal-Regulated MAP Kinases Pathology Janus Kinase 1 Phosphatidylinositol 3-Kinases Smad3 Protein Clinical Trial Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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