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Stromal Cell Derived Factor-1 (SDF-1) Targeting Reperfusion Reduces Myocardial Infarction in Isolated Rat Hearts SCIE SCOPUS

Title
Stromal Cell Derived Factor-1 (SDF-1) Targeting Reperfusion Reduces Myocardial Infarction in Isolated Rat Hearts
Authors
Jang, YHKim, JHBan, CAhn, KCheong, JHKim, HHKim, JSPark, YHKim, JChun, KJLee, GHKim, MKim, CXu, ZL
Date Issued
2012-10
Publisher
Blackwell Publishing
Abstract
Recent studies have shown that stromal cell derived factor-1 (SDF-1), first known as a cytokine involved in recruiting stem cells into injured organs, confers myocardial protection in myocardial infarction, which is not dependent on stem cell recruitment but related with modulation of ischemia-reperfusion (I/R) injury. However, the effect of SDF has been studied only in a preischemic exposure model, which is not clinically relevant if SDF is to be used as a therapeutic agent. Our study was aimed at evaluating whether or not SDF-1 confers cardioprotection during the reperfusion period. Hearts from SD rats were isolated and perfused with the Langendorff system. Proximal left coronary artery ligation, reperfusion, and SDF perfusion in KH buffer was done according to study protocol. Area of necrosis (AN) relative to area at risk (AR) was the primary endpoint of the study. Significant reduction of AN/AR by SDF in an almost dose-dependent manner was noted during both the preischemic exposure and reperfusion periods. In particular, infusion of a high concentration of SDF (25 nM/L) resulted in a dramatic reduction of infarct size, which was greater than that achieved with ischemic pre- or postconditioning. SDF perfusion during reperfusion was associated with a similar significant reduction of infarct size as preischemic SDF exposure. Further studies are warranted to assess the potential of SDF as a therapeutic agent for reducing I/R injury in clinical practice.
Keywords
Ischemic heart disease; SDF-1; ischemia reperfusion injury; myocardial infarction; STEM-CELLS; ISCHEMIA/REPERFUSION INJURY; FACTOR-1-ALPHA; RECRUITMENT; MOBILIZATION; SURVIVAL; DISEASE; CXCR4; SIZE; AXIS
URI
https://oasis.postech.ac.kr/handle/2014.oak/27503
DOI
10.1111/J.1755-5922.2011.00301.X
ISSN
1755-5914
Article Type
Article
Citation
CARDIOVASCULAR THERAPEUTICS, vol. 30, no. 5, page. 264 - 272, 2012-10
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반창일BAN, CHANGILL
Dept of Chemistry
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