NDLI: Beta-catenin promotes survival of renal epithelial cells by inhibiting Bax.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Zhiyong Havasi, Andrea Gall, Jonathan M. Mao, Haiping Schwartz, John H. Borkan, Steven C.
Description	Country affiliation: United States Author Affiliation: Wang Z ( Renal Section, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts, USA.)
Abstract	Ischemia activates Bax, a proapoptotic BCL2 protein, as well as the prosurvival beta-catenin/Wnt signaling pathway. To test the hypothesis that beta-catenin/Wnt signaling regulates Bax-mediated apoptosis after induction of metabolic stress, which occurs during renal ischemia, we infected immortalized and primary proximal tubular epithelial cells with adenovirus to express either constitutively active or dominant negative beta-catenin constructs. Constitutively active beta-catenin significantly decreased apoptosis and improved cell survival after metabolic stress. Furthermore, active beta-catenin decreased Bax activation, oligomerization, and translocation to mitochondria, and reduced both organelle membrane injury and apoptosis. Dominant negative beta-catenin had the opposite effects. Because Akt regulates Bax, we examined the effects of the beta-catenin mutants on Akt expression and activation. Constitutively active beta-catenin increased Akt-1 expression and activation before and after stress, and treatment with a phosphatidylinositol-3 kinase inhibitor antagonized the protective effects of beta-catenin on Akt activation, Bax inhibition, and cell survival. In addition, beta-catenin significantly increased the rate of phosphorylation at Bax serine(184), an Akt-specific target. Taken together, these results suggest that beta-catenin/Wnt signaling promotes survival of renal epithelial cells after metabolic stress, in part by inhibiting Bax in a phosphatidylinositol-3 kinase/Akt-dependent manner.
File Format	HTM / HTML
ISSN	10466673
e-ISSN	15333450
DOI	10.1681/ASN.2009030253
Journal	Journal of the American Society of Nephrology
Issue Number	9
Volume Number	20
Language	English
Publisher	American Society of Nephrology
Publisher Date	2009-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Nephrology Epithelial Cells Cytology Metabolism Kidney Tubules, Proximal Bcl-2-associated X Protein Beta Catenin Adenoviridae Genetics Animals Apoptosis Physiology Cell Line, Transformed Cell Survival Genes, Reporter Mice Mice, Inbred C57bl Mitochondria Phosphatidylinositol 3-kinases Proto-oncogene Proteins C-akt Signal Transduction Stress, Physiological Wnt Proteins Antagonists & Inhibitors Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Nephrology

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