help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Juncos, J. P.
Right arrow Articles by Nath, K. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Juncos, J. P.
Right arrow Articles by Nath, K. A.
(American Journal of Pathology. 2006;169:21-31.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.051195

Anomalous Renal Effects of Tin Protoporphyrin in a Murine Model of Sickle Cell Disease

Julio P. Juncos*, Joseph P. Grande{dagger}, Narayana Murali*, Anthony J. Croatt*, Luis A. Juncos*, Robert P. Hebbel{ddagger}, Zvonimir S. Katusic§ and Karl A. Nath*

From the Division of Nephrology and Hypertension,* the Department of Pathology,{dagger} and the Department of Anesthesiology and Molecular Pharmacology and Experimental Therapeutics,§ Mayo Clinic College of Medicine, Rochester, Minnesota; and the Vascular Biology Center and the Division of Hematology, Oncology, and Transplantation,{ddagger} University of Minnesota, Minneapolis, Minnesota

In human and murine models of sickle cell disease (SCD), heme oxygenase-1 (HO-1) is induced in the kidney, an organ commonly involved in SCD. The present study assessed the role of HO-1 by using a competitive inhibitor of HO activity, tin protoporphyrin (SnPP), in protocols affording a composite, clinically relevant analysis of the kidney in SCD under unstressed and stressed conditions. Whereas short-term administration of SnPP exerted comparable renal hemodynamic effects in wild-type and sickle mice, chronic administration of SnPP exerted divergent effects: SnPP provoked tubulointerstitial inflammation and up-regulation of injury-related genes in wild-type mice, whereas in sickle mice SnPP reduced expression of injury-related genes and vascular congestion without provoking tubulointerstitial inflammation. SnPP also protected against the heightened sensitivity to renal ischemia observed in sickle mice, preventing ischemia-induced worsening of renal injury in sickle mice above that observed in wild-type mice. Effective and comparable inhibition of HO activity by SnPP in wild-type and sickle mice was confirmed. These findings suggest that induction of HO-1, at least as assessed by this approach, may contribute to renal injury in this murine model of SCD and uncover an experimental maneuver that protects the kidney in murine SCD.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
K. A. Nath, L. V. d'Uscio, J. P. Juncos, A. J. Croatt, M. C. Manriquez, S. T. Pittock, and Z. S. Katusic
An analysis of the DOCA-salt model of hypertension in HO-1-/- mice and the Gunn rat
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H333 - H342.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
N. Hill-Kapturczak and A. Agarwal
Haem oxygenase-1--a culprit in vascular and renal damage?
Nephrol. Dial. Transplant., June 1, 2007; 22(6): 1495 - 1499.
[Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
M. J. Tracz, J. P. Juncos, J. P. Grande, A. J. Croatt, A. W. Ackerman, G. Rajagopalan, K. L. Knutson, A. D. Badley, M. D. Griffin, J. Alam, et al.
Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1-/- Mice
Am. J. Pathol., June 1, 2007; 170(6): 1820 - 1830.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Society for Investigative Pathology.