NDLI: Simultaneous deletion of Bax and Bak is required to prevent apoptosis and interstitial fibrosis in obstructive nephropathy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jang, Hee-Seong Padanilam, Babu J.
Description	Author Affiliation: Jang HS ( Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska); Padanilam BJ ( Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska)
Abstract	Proximal tubular injury and apoptosis are key mediators of the development of kidney fibrosis, a hallmark of chronic kidney disease. However, the molecular mechanism by which tubular apoptotic cell death leads to kidney fibrosis is poorly understood. In the present study, we tested the roles of Bcl-2-associated X (Bax) and Bcl-2 antagonist/killer (Bak), two crucial proteins involved in intrinsic apoptotic cell death, in the progression of kidney fibrosis. Mice with proximal tubule-specific Bax deletion, systemic deletion of Bak, and dual deletion of Bax and Bak were subjected to unilateral ureteral obstruction (UUO). Dual deficiency of Bax and Bak inhibited tubular apoptosis and atrophy. Consistent with decreased tubular injury, dual ablation of Bax and Bak suppressed UUO-induced inflammation and kidney fibrosis with decreased tubular cell cycle arrest, expression of fibrogenic and inflammatory cytokines, and oxidative stress in the kidney. Bax or Bak deficiency was insufficient to prevent apoptosis and all other aforementioned malevolent effects, suggesting compensatory mediation by each other in the respective signaling pathways. These data suggest that dual ablation of Bax and Bak in the kidney is required to prevent UUO-induced tubular apoptosis and the consequent kidney inflammation and fibrosis.
File Format	HTM / HTML
ISSN	1931857X
e-ISSN	15221466
DOI	10.1152/ajprenal.00170.2015
Journal	AJP: Renal Physiology
Issue Number	6
Volume Number	309
Language	English
Publisher	American Physiological Society
Publisher Date	2015-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Kidney Diseases Bcl-2 Homologous Antagonist-killer Protein Kidney Tubules Mice, Inbred C57bl Discipline Nephrology Metabolism Kidney Mice, Knockout Discipline Physiology Pathology Ureteral Obstruction Animals Collagen Gene Deletion Fibrosis Bcl-2-associated X Protein Genetics Mice Lipid Peroxidation Apoptosis
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

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