NDLI: WISP1, a pro-mitogenic, pro-survival factor, mediates tumor necrosis factor-alpha (TNF-alpha)-stimulated cardiac fibroblast proliferation but inhibits TNF-alpha-induced cardiomyocyte death.

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WISP1, a pro-mitogenic, pro-survival factor, mediates tumor necrosis factor-alpha (TNF-alpha)-stimulated cardiac fibroblast proliferation but inhibits TNF-alpha-induced cardiomyocyte death.

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WISP1, a pro-mitogenic, pro-survival factor, mediates tumor necrosis factor-alpha (TNF-alpha)-stimulated cardiac fibroblast proliferation but inhibits TNF-alpha-induced cardiomyocyte death.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Venkatachalam, Kaliyamurthi Valente, Anthony J. Clark, Robert A. Melby, Peter C. Nandish, Sailesh Chandrasekar, Bysani Venkatesan, Balachandar Reusch, Jane E. B.
Description	Author Affiliation: Venkatachalam K ( Department of Veterans Affairs, South Texas Veterans Health Care System, TX 78229, USA.)
Abstract	WNT1-inducible signaling pathway protein-1 (WISP1), a member of the CYR61/CTGF/Nov family of growth factors, can mediate cell growth, transformation, and survival. Previously we demonstrated that WISP1 is up-regulated in post-infarct heart, stimulates cardiac fibroblast proliferation, and is induced by the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). Here we investigated (i) the localization of TNF-alpha and WISP1 in post-infarct heart, (ii) the mechanism of TNF-alpha-mediated WISP1 induction in primary human cardiac fibroblasts (CF), (iii) the role of WISP1 in TNF-alpha-mediated CF proliferation and collagen production, and (iv) the effects of WISP1 on TNF-alpha-mediated cardiomyocyte death. TNF-alpha and WISP1 expressions were increased in the border zones and non-ischemic remote regions of the post-ischemic heart. In CF, TNF-alpha potently induced WISP1 expression in cyclic AMP response element-binding protein (CREB)-dependent manner. TNF-alpha induced CREB phosphorylation in vitro and DNA binding and reporter gene activities in vivo. TNF-alpha induced CREB activation via ERK1/2, and inhibition of ERK1/2 and CREB blunted TNF-alpha-mediated WISP1 induction. Most importantly, WISP1 knockdown attenuated TNF-alpha stimulated collagen production and CF proliferation. Furthermore, WISP1 attenuated TNF-alpha-mediated cardiomyocyte death, thus demonstrating pro-mitogenic and pro-survival effects for WISP1 in myocardial constituent cells. Our results suggest that a TNF-alpha/WISP1 signaling pathway may contribute to post-infarct cardiac remodeling, a condition characterized by fibrosis and progressive cardiomyocyte loss.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	21
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-05-22
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Fibroblasts Cytology Intracellular Signaling Peptides And Proteins Metabolism Mitogens Myocytes, Cardiac Oncogene Proteins Proto-Oncogene Proteins Tumor Necrosis Factor-alpha Animals CCN Intercellular Signaling Proteins Cell Death Drug Effects Cell Proliferation Cell Survival Cells, Cultured Collagen Biosynthesis Cyclic AMP Response Element-Binding Protein Enzymology Genetics Mice Mitogen-Activated Protein Kinases Molecular Sequence Data Myocardial Infarction Pathology NF-kappa B Protein Transport Transcription, Genetic Pharmacology Research Support, U.S. Gov't, Non-P.H.S. Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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