Kiani Ali Asghar, Babaei Fereshteh, Sedighi Mehrnoosh, Soleimani Azam, Ahmadi Kolsum, Shahrokhi Somayeh, Anbari Khatereh, Nazari Afshin
Razi Herbal Medicines Research Center and School of Allied Medical Sciences, Department of Hematology and Blood Transfusion, Lorestan University of Medical Sciences, Khorramabad, Iran.
Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran.
Iran J Basic Med Sci. 2017 Jun;20(6):648-654. doi: 10.22038/IJBMS.2017.8832.
Experimental myocardial infarction triggers secretion of Stromal cell-derived factor1 and lead to increase in the expression of its receptor "CXCR4" on the surface of various cells. The aim of this study was to evaluate the expression pattern of CXCR4 in peripheral blood cells following time-course permanent and temporary ischemia in rats.
Fourteen male Wistar rats were divided into two groups of seven and were placed under permanent and transient ischemia. Peripheral blood mononuclear cells were isolated at different time points, RNAs extracted and applied to qRT-PCR analysis of the CXCR4 gene.
Based on repeated measures analysis of variance, the differences in the expression levels of the gene in each of the groups were statistically significant over time (the effect of time) (<0.001). Additionally, the difference in gene expression between the two groups was statistically significant (the effect of group), such that at all times, the expression levels of the gene were significantly higher in the permanent ischemia than in the transient ischemia group (<0.001). Moreover, the interactive effect of time-group on gene expression was statistically significant (<0.001).
CXCR4 is modulated in an induced ischemia context implying a possible association with myocardial infarction. Checking of CXCR4 expression in the ischemic changes shows that damage to the heart tissue trigger the secretion of inflammatory chemokine SDF, Followed by it CXCR4 expression in blood cells. These observations suggest that changes in the expression of CXCR4 may be considered a valuable marker for monitoring myocardial infarction.
实验性心肌梗死会触发基质细胞衍生因子1的分泌,并导致其受体“CXCR4”在各种细胞表面的表达增加。本研究的目的是评估大鼠永久性和暂时性缺血随时间变化后外周血细胞中CXCR4的表达模式。
将14只雄性Wistar大鼠分为两组,每组7只,分别置于永久性和暂时性缺血状态。在不同时间点分离外周血单核细胞,提取RNA并应用于CXCR4基因的qRT-PCR分析。
基于重复测量方差分析,各时间点两组基因表达水平差异有统计学意义(时间效应)(<0.001)。此外,两组间基因表达差异有统计学意义(组效应),即永久性缺血组基因表达水平在各个时间点均显著高于暂时性缺血组(<0.001)。而且,时间-组对基因表达的交互作用有统计学意义(<0.001)。
CXCR4在缺血诱导的情况下受到调节,这意味着它可能与心肌梗死有关。检查缺血变化中CXCR4的表达表明,心脏组织损伤会触发炎症趋化因子SDF的分泌,随后血细胞中CXCR4表达增加。这些观察结果表明,CXCR4表达的变化可能被视为监测心肌梗死的一个有价值的标志物。