Cyclooxygenase-2 in the kidney: good, BAD, or both?

• Type of Material: Article
• Authors: Russ Price, Emory University; Janet D Klein, Emory University
• Language: English
• Date: 2011-11
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2011 International Society of Nephrology
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://www.nature.com/ki/journal/v80/n9/full/ki2011263a.html
• Title of Journal or Parent Work: Kidney International
• ISSN: 0085-2538
• Volume: 80
• Issue: 9
• Start Page: 905
• End Page: 907
• Grant/Funding Information: This work was supported by US National Institutes of Health grants DK50740 (to S.R.P.) and DK41707 (to J.D.K.).
• Research Categories: Health Sciences, General; Health Sciences, Medicine and Surgery; Biology, Physiology

Abstract

Hypertonic stress in the kidney inner medulla is common, yet inner medullary cells adapt to limit cell death. Küper et al. have identified a cell-survival response by which increased cyclooxygenase-2 (COX-2) stimulates a prostaglandin E2 (PGE2)/ protein kinase A (PKA)-mediated inactivation of the pro-apoptotic protein BAD. However, the PGE2/PKA pathway is not the only means to inactivate BAD and limit cell death. This Commentary shows a broader picture of this pathway to examine the kidney's BAD options.