Cardioprotective effects of monocyte locomotion inhibitory factor on myocardial ischemic injury by targeting vimentin

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• 作者：Shu Jiang^a ; ^c ; ¹ ; Yulan Liu^a ; ¹ ; Jing Wang^b ; Yue Zhang^b ; Yaocheng Rui^a ; Yuefan Zhang^a ; ^{zhangyuefan@126.com} ; Tiejun Li^a ; ^c ; ^{ltj204@163.com}
• 关键词：MLIF ; monocyte locomotion inhibitory factor ; ICAM-1 ; intercellular cell adhesion molecule-1 ; VCAM-1 ; vascular cell adhesion molecule-1 ; eEF1A1 ; eukaryotic translation elongation factor 1 alpha 1 ; eEF1A2 ; eukaryotic translation elongation factor 1 alpha 2 ; eNOS ; endothelial nitric oxide synthase ; MALDI-TOF-MS ; matrix assisted laser desorption- ionization time of flight- mass spectrometry
• 刊名：Life Sciences
• 出版年：2016
• 出版时间：15 December 2016
• 年：2016
• 卷：167
• 期：Complete
• 页码：85-91
• 全文大小：1025 K
• 卷排序：167

文摘

Monocyte locomotion inhibitory factor (MLIF), a heat-stable pentapeptide produced by Entamoeba histolytica, has anti-inflammatory function and protective effect on ischemic stroke. In this study, we evaluated the effect of MLIF on myocardial ischemia. Mice were subjected to ischemia/reperfusion by occlusion of the left anterior descending artery (LAD). After sacrifice, the serum concentrations of cardiac troponin I (cTnI), creatine kinase (CK), lactate dehydrogenase (LDH) as well as the heart infarct size were measured. HE and TUNEL staining were used to observe the pathological damage and the apoptotic cells. For in vitro study, the oxygen-glucose deprivation(OGD) model was established in H9c2 cells. MTT assay and flow cytometry assay were performed to evaluate cell viability and apoptosis. The expression of JNK and caspase 3 was assessed by western blot analysis. Pull-down assay was used to detect the specific binding protein of MLIF in myocardial cells. MLIF significantly reduced the infarct size, and the cTnI, CK and LDH levels, amelioratived pathological damage and reduced the apopotosis compared with the myocardial I/R model group. MLIF improved cell survival and inhibited apoptosis and necrosis by inhibiting the p-JNK and cleaved caspase3 expression. Furthermore, the binding protein of MLIF in myocardial cells was vimentin. Inhibition of vimentin expression by withaferin A or vimentin siRNA repressed the protective effects of MLIF in OGD-provoked H9c2 cells. Taken together, our results demonstrate that the cardioprotective effects of MLIF on myocardial ischemia injury are related to reductions in the inflammatory response and apoptosis by targeting vimentin.