Effects of Ischemic Preconditioning in the Late Phase on Homing of Endothelial Progenitor Cells in Renal Ischemia/Reperfusion Injury

2013 ◽  
Vol 45 (2) ◽  
pp. 511-516 ◽  
Author(s):  
C.-J. Bo ◽  
B. Chen ◽  
R.-P. Jia ◽  
J.-G. Zhu ◽  
P. Cao ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Late Phase ◽  
Renal Ischemia ◽  
Endothelial Progenitor ◽  
Renal Ischemia Reperfusion Injury

Ischemic preconditioning improved renal ischemia/reperfusion injury and hyperglycemia

IUBMB Life ◽  
2018 ◽  
Vol 71 (3) ◽  
pp. 321-329 ◽  
Author(s):  
Jian-Ri Li ◽  
Yen-Chuan Ou ◽  
Chih-Cheng Wu ◽  
Jiaan-Der Wang ◽  
Shih-Yi Lin ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

Dynamics of mobilization and homing of endothelial progenitor cells after acute renal ischemia: modulation by ischemic preconditioning

2006 ◽  
Vol 291 (1) ◽  
pp. F176-F185 ◽  
Author(s):  
Daniel Patschan ◽  
Krystina Krupincza ◽  
Susann Patschan ◽  
Zhongtao Zhang ◽  
Carl Hamby ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Ischemic Preconditioning ◽  
Fluorescent Protein ◽  
Late Phase ◽  
Immunohistochemical Analysis ◽  
Renal Ischemia ◽  
Endothelial Progenitor ◽  
Ischemic Episode ◽  
Acute Renal Ischemia

Endothelial progenitor cells (EPCs) have been shown to participate in tissue repair under diverse physiological and pathological conditions. It is unknown whether EPCs are mobilized in response to acute renal injury. The aim of this study was to characterize EPC mobilization and homing in the course of acute renal ischemia. Mice were subjected to unilateral renal artery clamping (UC) for 25 min. At 10 min, 3, 6, 24 h, and 7 days after UC, the pool of circulating and splenic CD34+/Flk-1+ cells within the monocytic population was detected by flow cytometry. For ischemic preconditioning (IPC), the first UC was performed 7 days before the repeated ischemic episode. For EPC detection in the kidney, cryosections were stained for c-Kit+/Tie-2+ cells. The number of circulating EPCs was not significantly affected at any time after UC compared with sham-operated or control mice. IPC did not significantly change the circulating pool of EPCs. Splenectomy performed before UC resulted in a surge of circulating EPCs. Accordingly, splenic EPCs were significantly increased after UC at 3 and 6 h, but not at later times. EPC homing to the spleen was absent in IPC animals. Immunohistochemical analysis of the kidneys showed a sixfold increase in the number of c-Kit+/Tie-2+ cells localized in the medullopapillary region in mice by day 7 after ischemia. Enriched population of c-Kit+/Tie-2+ cells from the medullopapillary parenchyma of Tie-2green fluorescent protein chimeric mice subjected to IPC was isolated and transplanted to wild-type mice with acute renal ischemia. This procedure resulted in the improvement of renal function in recipients. In conclusion, 1) renal ischemia rapidly (within 3–6 h) mobilizes EPCs, which transiently home to the spleen, acting as a temporary reservoir of mobilized EPCs; 2) the late phase of IPC is associated with the mobilization of the splenic pool and accumulation of EPCs in the renal medullopapillary region; and 3) transplantation of EPC-enriched cells from the medullopapillary parenchyma afforded partial renoprotection after renal ischemia, suggesting the role of the recruited EPCs in the functional rescue.

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