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Highlights • FKN involves in the inflammatory and remodeling processes after AMI. • FKN is negative correlated with myocardial salvage in STEMI patients underwent PCI. • Higher FKN level after primary PCI predicts worse MACE events in AMI patients. Abstract Background Recent studies demonstrated that fractalkine (FKN) is critically involved in the regulation of inflammation and cardiac function. Objective This study aimed to investigate the prognostic value of circulating FKN in patients with ST-elevated acute myocardial infarction (STEMI) after primary PCI. Methods We enrolled ninety consecutive STEMI patients and investigated the association of circulating FKN with myocardial salvage and the occurrence of major adverse cardiac events (MACE) after PCI. Results During a median follow-up of 387 days, total 15 MACE (16.67%) were registered in the study population. Patients with MACE were more likely to be occurred in elderly patients with 3-vessel disease. Correlation analysis demonstrated the level of FKN at day 1 after PCI (FKN@day-1) not only significantly correlated with the levels of hs-TnT at day 7 after PCI (R2 = 0.06; p = 0.02) but inversely correlated with the measurements of LVEF at 1-month observation (R2 = 0.10; p = 0.00). Kaplan-Meier survival analyses further revealed that patients with the level of FKN@day-1 above the median had a higher incidence of MACE compared with those whose FKN@day-1 levels below the median (log-rank test x2 = 13.29, p < 0.001). In addition, multivariate Cox regression analysis demonstrated that FKN@day-1 was an independent predictor of MACE (hazard ratio: 4.63; 95% confidence interval: 1.53–14.01; p = 0.00), together with WBC count and 3-vessel disease for STEMI patients. Conclusions Our study demonstrates that FKN@day-1 is negative correlated with myocardial salvage after acute myocardial infarction and might be a valuable prognostic marker of MACE in patients with STEMI undergone PCI. [ABSTRACT FROM AUTHOR]

Poor cell survival post transplantation compromises the therapeutic benefits of mesenchymal stem cells (MSCs) in myocardial infarction (MI). Hepatocyte growth factor (HGF) is an important cytokine for angiogenesis, anti-inflammation and anti-apoptosis. This study aimed to evaluate the cardioprotective effects of MSCs overexpressing HGF in a mouse model of MI. The apoptosis of umbilical cord-derived MSCs (UC-MSCs) and HGF-UC-MSCs under normoxic and hypoxic conditions was detected. The conditioned medium (CdM) of UC-MSCs and HGF-UC-MSCs under a hypoxic condition was harvested and its protective effect on neonatal cardiomyocytes (NCMs) exposed to a hypoxic challenge was examined. UC-MSCs and HGF-UC-MSCs were transplanted into the peri-infarct region in mice following MI and heart function assessed 4 weeks post transplantation. The apoptosis of HGF-UC-MSCs under hypoxic conditions was markedly decreased compared with that of UC-MSCs. NCMs treated with HGF-UC-MSC hypoxic CdM (HGF-UC-MSCs-hy-CdM) exhibited less cell apoptosis in response to hypoxic challenge than those treated with UC-MSC hypoxic CdM (UC-MSCs-hy-CdM). HGF-UC-MSCs-hy-CdM released the inhibited p-Akt and lowered the enhanced ratio of Bax/Bcl-2 induced by hypoxia in the NCMs. HGF-UC-MSCs-hy-CdM expressed higher levels of HGF, EGF, bFGF and VEGF than UC-MSCs-hy-CdM. Transplantation of HGF-UC-MSCs or UC-MSCs greatly improved heart function in the mouse model of MI. Compared with UC-MSCs, transplantation of HGF-UC-MSCs was associated with less cardiomyocyte apoptosis, enhanced angiogenesis and increased proliferation of cardiomyocytes. This study may provide a novel therapeutic strategy for MSC-based therapy in cardiovascular disease. [ABSTRACT FROM AUTHOR]