Abstract
ObjectiveTo investigate the effects of circulating microvesicles derived from myocardial ischemia (I-MVs) on apoptosis in myocardial ischemia/reperfusion (I/R) injury in rats.MethodsI-MVs from rats undergoing myocardial left anterior descending (LAD) coronary artery ligation were isolated by ultracentrifugation from circulating blood and characterized by flow cytometry. I-MVs were administered intravenously (4.8 mg/kg) at 5 min before reperfusion procedure in I/R injury model which was induced by 30-min of ischemia and 120-min of reperfusion of LAD in rats.ResultsTreatment with I-MVssignificantly reduced the size of myocardial infarction, the activities of serum CK-MB and LDH, and the number of apoptotic cardiomyocytes. The activities of caspase 3, caspase 9 and caspase 12 in myocardium were also decreased significantly with I-MVs treatment. Moreover, the expression of Bax was decreased but Bcl-2 was increased. The expression of glucose regulated protein 78 (GRP78), sarco/endoplasmic reticulum Ca2+-ATPase 2 (SERCA2) and phosphorylated phospholamban (p-PLB) were increased after being treated with I-MVs.ConclusionI-MVs could protect hearts from I/R injury in rats through SERCA2 and p-PLB of calcium regulatory proteins to alleviate intrinsic myocardial apoptosis including mitochondrial and endoplasmic reticulum pathways.
Highlights
Microvesicles (MVs) are small vesicles of 0.1~1μm in diameter and deriving from the shedding of cellular membrane during activation or apoptosis
I/R injury model in vivo in rats was established successfully according to the changes of heart rate (HR), mean arterial pressure (MAP) and ST-T segment throughout the whole process of experiment and ventricular arrhythmia (VA) during ischemia period
HR was increased, MAP was elevated and ST-segment was fallen after reperfusion
Summary
Microvesicles (MVs) are small vesicles of 0.1~1μm in diameter and deriving from the shedding of cellular membrane during activation or apoptosis. Recent studies indicated that patients with cardiovascular diseases such as ischemia heart disease, atherosclerosis, hypertension have increased circulating levels of MVs [4]. This suggested that under pathological states, MVs may play a part in these processes. Jeanneteau et al showed MVs from rats and healthy humans undergoing remote ischemic conditioning (RCond) increased in circulating levels of EMVs and PMVs. injecting RCondderived MVs to I/R injury rats before reperfusion did not induce cardioprotection [8]. It is of important realistic meaning to research the effects of MVs derived from ischemic myocardium especially on apoptosis in myocardial I/R injury How about I-MVs? So it is of important realistic meaning to research the effects of MVs derived from ischemic myocardium especially on apoptosis in myocardial I/R injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
