| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Urology and Surgery, Johns Hopkins University, Baltimore, Maryland 21287
Heat shock produces cellular tolerance to a variety of adverse conditions; however, the protective effect of heat shock on renal cell ischemic injury remains unclear. Protein kinase C (PKC) has been implicated in the signaling mechanisms of acute preconditioning, yet it remains unknown whether PKC mediates heat shock-induced delayed preconditioning in renal cells. To study this, renal tubular cells (LLC-PK1) were exposed to thermal stress (43°C) for 1 h and heat shock protein (HSP) 72 induction was confirmed by Western blot analysis. Cells were subjected to simulated ischemia 24 h after thermal stress, and the effect of heat shock (delayed preconditioning) on ischemia-induced apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling) and B cell lymphoma 2 (Bcl2) expression (Western) was determined. Subsequently, the effect of PKC inhibition on HSP72 induction and heat stress-induced ischemic tolerance was evaluated. Thermal stress induced HSP72 production, increased Bcl2 expression, and prevented simulated ischemia-induced renal tubular cell apoptosis. PKC inhibition abolished thermal induction of HSP72 and prevented heat stress-induced ischemic tolerance. These data demonstrate that thermal stress protects renal tubular cells from simulated ischemia-induced apoptosis through a PKC-dependent mechanism.
kidney; preconditioning; hypoxia; B cell lymphoma 2
This article has been cited by other articles:
|
|
 |
|
  S. D. Coaxum, T. M. Griffin, J. L. Martin, and R. Mestril Influence of PKC-{alpha} overexpression on HSP70 and cardioprotection Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2220 - H2226. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Jeyaraj, D. Dakhlallah, S. R. Hill, and B. S. Lee Expression and distribution of HuR during ATP depletion and recovery in proximal tubule cells Am J Physiol Renal Physiol, December 1, 2006; 291(6): F1255 - F1263. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Pitcher, M. Wang, B. M. Tsai, A. Kher, N. T. Nelson, and D. R. Meldrum Endogenous estrogen mediates a higher threshold for endotoxin-induced myocardial protection in females Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R27 - R33. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Kher, K. K. Meldrum, K. L. Hile, M. Wang, B. M. Tsai, M. W. Turrentine, J. W. Brown, and D. R. Meldrum Aprotinin improves kidney function and decreases tubular cell apoptosis and proapoptotic signaling after renal ischemia-reperfusion J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 662 - 662. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. J. Padanilam Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis Am J Physiol Renal Physiol, April 1, 2003; 284(4): F608 - F627. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. K. Meldrum, A. L. Burnett, X. Meng, R. Misseri, M. B.K. Shaw, J. P. Gearhart, and D. R. Meldrum Liposomal Delivery of Heat Shock Protein 72 Into Renal Tubular Cells Blocks Nuclear Factor-{kappa}B Activation, Tumor Necrosis Factor-{alpha} Production, and Subsequent Ischemia-Induced Apoptosis Circ. Res., February 21, 2003; 92(3): 293 - 299. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
