A Meta-Analysis of Circulating Microvesicles in Patients with Myocardial
            Infarction

Wang, Zhida; Cai, Wenjing; Hu, Shaolan; Xia, Yu-fei; Wang, Yao; Zhang, Qi; Chen, Liming

doi:10.5935/abc.20170102

Cited by 4 publications

(1 citation statement)

References 29 publications

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“…In a porcine model of IR, we found that Ivabradine improved cardiac function after 7 days of reperfusion, in which a significant amount of plasma released MVs was detected. Intracardial release of extracellular vesicles, characterized as exosomes and microvesicles, are induced in response to acute myocardial infarction [ 19 , 20 ], suggesting that plasma circulating microvesicles are markers of progression of infarction [ 19 , 20 , 21 , 22 , 23 ]. Injection of Ivabradine-induced Plasma MVs isolated 7 days after IR mimicked the effect of Ivabradine in pigs subjected to acute myocardial infarction, suggesting that at least, Ivabradine may induce cardiac protection by releasing cardiac specific MVs.…”

Section: Discussionmentioning

confidence: 99%

Ivabradine-Stimulated Microvesicle Release Induces Cardiac Protection against Acute Myocardial Infarction

Ramírez-Carracedo

Tesoro

Hernández

et al. 2020

IJMS

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Ivabradine can reduce heart rate through inhibition of the current I(f) by still unexplored mechanisms. In a porcine model of ischemia reperfusion (IR), we found that treatment with 0.3 mg/kg Ivabradine increased plasma release of microvesicles (MVs) over Placebo, as detected by flow cytometry of plasma isolated from pigs 7 days after IR, in which a tenfold increase of Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) containing (both high and low-glycosylated) MVs, was detected in response to Ivabradine. The source of MVs was investigated, finding a 37% decrease of CD31+ endothelial cell derived MVs, while CD41+ platelet MVs remained unchanged. By contrast, Ivabradine induced the release of HCN4+ (mostly cardiac) MVs. While no differences respect to EMMPRIN as a cargo component were found in endothelial and platelet derived MVs, Ivabradine induced a significant release of EMMPRIN+/HCN4+ MVs by day 7 after IR. To test the role of EMMPRIN+ cardiac MVs (EMCMV), H9c2 cell monolayers were incubated for 24 h with 107 EMCMVs, reducing apoptosis, and increasing 2 times cell proliferation and 1.5 times cell migration. The in vivo contribution of Ivabradine-induced plasma MVs was also tested, in which 108 MVs isolated from the plasma of pigs treated with Ivabradine or Placebo 7 days after IR, were injected in pigs under IR, finding a significant cardiac protection by increasing left ventricle ejection fraction and a significant reduction of the necrotic area. In conclusion ivabradine induces cardiac protection by increasing at least the release of EMMPRIN containing cardiac microvesicles.

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