Ischemic preconditioning increases endothelial progenitor cell number to attenuate partial nephrectomy-induced ischemia/reperfusion injury

The objective of this study was to investigate the role of endothelial progenitor cells (EPCs) in the modulation of ischemia-reperfusion injury (IRI) in a partial nephrectomy (PN) rat model using early-phase ischemic preconditioning (IPC). Ninety male Sprague-Dawley rats were randomly divided into t...

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Veröffentlicht in:PloS one 2013-01, Vol.8 (1), p.e55389-e55389
Hauptverfasser: Liu, Hao, Wu, Ran, Jia, Rui-Peng, Zhong, Bing, Zhu, Jia-Geng, Yu, Peng, Zhao, Yan, Ge, Yu-Zheng, Wu, Jian-Ping
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container_title PloS one
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creator Liu, Hao
Wu, Ran
Jia, Rui-Peng
Zhong, Bing
Zhu, Jia-Geng
Yu, Peng
Zhao, Yan
Ge, Yu-Zheng
Wu, Jian-Ping
description The objective of this study was to investigate the role of endothelial progenitor cells (EPCs) in the modulation of ischemia-reperfusion injury (IRI) in a partial nephrectomy (PN) rat model using early-phase ischemic preconditioning (IPC). Ninety male Sprague-Dawley rats were randomly divided into three groups following right-side nephrectomy: Sham-operated rats (surgery without vascular clamping); PN rats (renal blood vessels were clamped for 40 min and PN was performed); and IPC rats (pretreated with 15 min ischemia and 10 min reperfusion). At 1, 3, 6, 12, 24 h, and 3 days after reperfusion, the pool of circulating EPCs and kidneys were harvested. The extent of renal injury was assessed, along with EPC number, cell proliferation, angiogenesis, and vascular growth factor expression. Pretreated rats exhibited significant improvements in renal function and morphology. EPC numbers in the kidneys were increased at 12 h following reperfusion in the IPC group as compared to the PN or Sham groups. Cell proliferation (including endothelial and tubular epithelial cells) and angiogenesis in peritubular capillaries were markedly increased in kidneys treated with IPC. In addition, vascular endothelial growth factor-A (VEGF-A) and stromal cell-derived factor-1α (SDF-1α) expression in the kidneys of pretreated rats was increased compared to rats subjected to PN. OUR INVESTIGATION SUGGESTED THAT: (1) the early phase of IPC may attenuate renal IRI induced by PN; (2) EPCs play an important role in renal protection, involving promotion of cell proliferation and angiogenesis through release of several angiogenic factors.
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Ninety male Sprague-Dawley rats were randomly divided into three groups following right-side nephrectomy: Sham-operated rats (surgery without vascular clamping); PN rats (renal blood vessels were clamped for 40 min and PN was performed); and IPC rats (pretreated with 15 min ischemia and 10 min reperfusion). At 1, 3, 6, 12, 24 h, and 3 days after reperfusion, the pool of circulating EPCs and kidneys were harvested. The extent of renal injury was assessed, along with EPC number, cell proliferation, angiogenesis, and vascular growth factor expression. Pretreated rats exhibited significant improvements in renal function and morphology. EPC numbers in the kidneys were increased at 12 h following reperfusion in the IPC group as compared to the PN or Sham groups. Cell proliferation (including endothelial and tubular epithelial cells) and angiogenesis in peritubular capillaries were markedly increased in kidneys treated with IPC. In addition, vascular endothelial growth factor-A (VEGF-A) and stromal cell-derived factor-1α (SDF-1α) expression in the kidneys of pretreated rats was increased compared to rats subjected to PN. 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control</subject><subject>Rodents</subject><subject>Stem cells</subject><subject>Stem Cells - physiology</subject><subject>Studies</subject><subject>Surgery</subject><subject>Urology</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Veins &amp; arteries</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk92K1TAUhYsozjj6BqIFQfTinGmSJk1vhGHw58DAgH-3IU132xzapCapeF7Bpzb1dIapzIX0oiX99lrdq3snyXOUbREp0PneTs7IfjtaA9sso5Tw8kFyikqCNwxn5OGd55Pkiff7CBHO2OPkBBPCCSry0-T3zqsOBq3S0YGyptZBW6NNm2qjHEgPPgVT29BBr2UfKduC0cG6VEHfp2YaKnBpsKkMAcwkA6SjdGFmDYxdFA12OGy0qScFdaqPdvLcwQiumXx0i1b7yR2eJo8a2Xt4ttzPkm8f3n-9_LS5uv64u7y42qiC8rCpS17hom5opijIiqIqplFWCpWsKCuMpEKsaSqGsgYjmudUISlVySpJEOeyImfJy6Pu2Fsvlhi9QATzDGesoJHYHYnayr0YnR6kOwgrtfh7YF0r5hZVDwIrhBVHUNQY5YSSimVlAVSxHCmOaxa13i1uUzVArcAEJ_uV6PqN0Z1o7U9BKEO4zKLAm0XA2R8T-CCGGGLMXhqwU_xuzHOGMSV5RF_9g97f3UK1MjagTWOjr5pFxUVeFCVmvMCR2t5DxauepyXOXKPj-arg7aogMgF-hVZO3ovdl8__z15_X7Ov77AdyD503vbTPKd-DeZHUDnrvYPmNmSUiXllbtIQ88qIZWVi2Yu7P-i26GZHyB8HuxTg</recordid><startdate>20130131</startdate><enddate>20130131</enddate><creator>Liu, Hao</creator><creator>Wu, Ran</creator><creator>Jia, Rui-Peng</creator><creator>Zhong, Bing</creator><creator>Zhu, Jia-Geng</creator><creator>Yu, Peng</creator><creator>Zhao, Yan</creator><creator>Ge, Yu-Zheng</creator><creator>Wu, Jian-Ping</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130131</creationdate><title>Ischemic preconditioning increases endothelial progenitor cell number to attenuate partial nephrectomy-induced ischemia/reperfusion injury</title><author>Liu, Hao ; 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Ninety male Sprague-Dawley rats were randomly divided into three groups following right-side nephrectomy: Sham-operated rats (surgery without vascular clamping); PN rats (renal blood vessels were clamped for 40 min and PN was performed); and IPC rats (pretreated with 15 min ischemia and 10 min reperfusion). At 1, 3, 6, 12, 24 h, and 3 days after reperfusion, the pool of circulating EPCs and kidneys were harvested. The extent of renal injury was assessed, along with EPC number, cell proliferation, angiogenesis, and vascular growth factor expression. Pretreated rats exhibited significant improvements in renal function and morphology. EPC numbers in the kidneys were increased at 12 h following reperfusion in the IPC group as compared to the PN or Sham groups. Cell proliferation (including endothelial and tubular epithelial cells) and angiogenesis in peritubular capillaries were markedly increased in kidneys treated with IPC. In addition, vascular endothelial growth factor-A (VEGF-A) and stromal cell-derived factor-1α (SDF-1α) expression in the kidneys of pretreated rats was increased compared to rats subjected to PN. OUR INVESTIGATION SUGGESTED THAT: (1) the early phase of IPC may attenuate renal IRI induced by PN; (2) EPCs play an important role in renal protection, involving promotion of cell proliferation and angiogenesis through release of several angiogenic factors.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23383174</pmid><doi>10.1371/journal.pone.0055389</doi><tpages>e55389</tpages><oa>free_for_read</oa></addata></record>
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subjects Analysis of Variance
Angiogenesis
Animals
Biology
Blood vessels
Blotting, Western
Bone marrow
Capillaries
Cell number
Cell proliferation
Cells (biology)
Chemokine CXCL12 - metabolism
Clamping
DNA Primers - genetics
Endothelial Cells - physiology
Endothelium
Epithelial cells
Flow Cytometry
Fluorescent Antibody Technique
Histological Techniques
Hospitals
Immunohistochemistry
Injuries
Ischemia
Ischemic Preconditioning - methods
Kidneys
Male
Medicine
Neovascularization, Physiologic - physiology
Nephrectomy
Nephrectomy - adverse effects
Polymerase Chain Reaction
Preconditioning
Progenitor cells
Rats
Rats, Sprague-Dawley
Renal function
Reperfusion
Reperfusion Injury - etiology
Reperfusion Injury - prevention & control
Rodents
Stem cells
Stem Cells - physiology
Studies
Surgery
Urology
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - metabolism
Veins & arteries
title Ischemic preconditioning increases endothelial progenitor cell number to attenuate partial nephrectomy-induced ischemia/reperfusion injury
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