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JCI online early table of contents: July 18, 2011
Date:7/18/2011

romoted slow-cycling progenitor cell proliferation, and this altered the properties of the slow-cycling progenitor cell niche. These data have important implications for understanding the airway injury and repair in individuals with CF.

TITLE: CGRP induction in cystic fibrosis airways alters the submucosal gland progenitor cell niche in mice

AUTHOR CONTACT:
John F. Engelhardt
The University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.
Phone: 319.335.7744; Fax: 319.335.7198; E-mail: john-engelhardt@uiowa.edu.

View this article at: http://www.jci.org/articles/view/41857?key=a930a26b5642a8148b4f


NEPHROLOGY: New mechanistic insight into salt-induced high blood pressure

High blood pressure (hypertension) is a risk factor for numerous severe medical conditions, including heart attack, stroke, and kidney failure. Increased sensitivity to salt is a contributing factor to high blood pressure in some individuals, but the underlying mechanism is not clear. Now, a team of researchers, led by Toshiro Fujita, at the University of Tokyo Graduate School of Medicine, Japan, has determined that high-salt loading activates the protein Rac1 in the kidneys in rodent models of salt-sensitive high blood pressure and that this elevates blood pressure and leads to kidney damage. The chain of events downstream of Rac1 activation required the protein MR (mineralocorticoid receptor). These data provide new insight into the mechanism underlying salt-induced high blood pressure and kidney injury, and provide potential new therapeutic targets for treating these conditions.

TITLE: Rac1 GTPase in rodent kidneys is essential for salt-sensitive hypertension via a mineralocorticoid receptordependent pathway

AUTHOR CONTACT:
Toshiro Fujita
University of Tokyo G
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Contact: Karen Honey
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Journal of Clinical Investigation
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