AJP - Renal AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol (January 24, 2006). doi:10.1152/ajprenal.00424.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
290/6/F1559    most recent
00424.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zahedi, K.
Right arrow Articles by Soleimani, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zahedi, K.
Right arrow Articles by Soleimani, M.
Submitted on October 25, 2005
Accepted on January 18, 2006

Stathmin Deficient Mice Develop Fibrosis and Show Delayed Recovery from Ischemic Reperfusion Injury

Kamyar Zahedi1*, Monica P. Revelo2, Sharon Barone3, Zhaohui Wang3, Kathy Tehrani1, David P. Citron1, John J. Bissler1, Hamid Rabb4, and Manoocher Soleimani5

1 Division of Nephrology and Hypertension, Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
2 Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
3 Division of Nephrology and Hypertension, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
4 Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
5 Division of Nephrology and Hypertension, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; Veteran Affairs Medical Center, Cincinnati, Ohio, USA

* To whom correspondence should be addressed. E-mail: kamyar.zahedi{at}cchmc.org.

In kidneys subjected to ischemic reperfusion injury (IRI) stathmin, a tubulin binding protein involved in the regulation of mitosis, is expressed in dedifferentiated and proliferating renal tubule cells during the recovery phase. To ascertain the role of stathmin in the recovery from ischemic kidnet injury stathmin deficient (OP18-/-) and wild type (WT) animals were subjected to experimental IRI. At 3, 7 and 14 days after reperfusion serum samples and kidneys were collected for the examination of parameters of renal function, morphology and recovery. Our studies indicate that on day 14 after reperfusion OP18-/- mice have significant renal failure whereas the creatinine levels of WT animals have returned to baseline. In comparison to WT animals OP18-/- mice had more extensive tubular fibrosis. The examination of proliferating cell nuclear antigen (PCNA) expression indicated that OP18-/- animals have increased proliferative or DNA repair activity for a more prolonged duration. The OP18-/- animals also had increased number of tubules with apoptotic cells. These results suggest that in stathmin deficient mice subjected to IRI, the aberrant regulation of cell cycle progression, not observed under normal conditions, impairs or at least delays the process of tubular repair and recovery after acute renal injury.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
C. Jayle, F. Favreau, K. Zhang, C. Doucet, J. M. Goujon, W. Hebrard, M. Carretier, M. Eugene, G. Mauco, J. P. Tillement, et al.
Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model
Am J Physiol Renal Physiol, March 1, 2007; 292(3): F1082 - F1093.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.