Protective effects of circulating microvesicles derived from myocardial ischemic rats on apoptosis of cardiomyocytes in myocardial ischemia/reperfusion injury

Wang, Yao; Wei, Su; Wang, Yilu; Liu, Miao; Shang, Ming; Zhang, Qi; Wu, Yongjian; Liu, Ming-Lin; Song, Jun-Qiu; Liu, Yanxia

doi:10.18632/oncotarget.17424

Cited by 11 publications

(11 citation statements)

References 31 publications

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“…MVs are cystic vesicles secreted from cells under stimulation or apoptosis, which can be involved in the pathogenesis of various diseases. Recent studies have demonstrated that circulating MVs are responsible for the transmission of IPC signals that elicit cardioprotection [5,6]. In the present study, IPC-MVs and Sham-MVs in circulation were successfully obtained, and the total amount of IPC-MVs was slightly higher than that of Sham-MVs.…”

Section: Discussionsupporting

confidence: 44%

“…It is wellknown that ischemic preconditioning (IPC) is one of the most powerful cardioprotective interventions to reduce myocardial I/R injury [2], which could induce extracellular vesicles (EVs) such as microvesicles (MVs) and exosomes release and changes in microRNA (miRNA) expression in cardiomyocytes [3,4], but the underlying mechanism remains elusive. Recently, it has been shown in our study that circulating MVs released from the heart after IPC (IPC-MVs) are required for cardioprotection by IPC [5] and that IPC-MVs could protect against myocardial I/R injury by regulating GRP78 and CHOP expression in endoplasmic reticulum pathway [6]. However, elucidating the protective mechanisms of IPC-MVs needs further molecular experimentation.…”

Section: Introductionmentioning

confidence: 88%

“…The myocardial I/R model was established by occluding the left anterior descending (LAD) coronary artery in rats for 30 min followed by 120 min reperfusion and IPC was induced by three cycles of 5 min ischemia and 5 min reperfusion of the LAD as previously described [5]. Successful occlusions were verified by observing the development of ST-segment elevation on electrocardiogram (ECG).…”

Section: Establishment Of the I/r And Ipc Model In Vivomentioning

confidence: 99%

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MiR-133a-3p transferred by circulating microvesicles derived from myocardial ischemic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury

Zhao

Zhu

Shang

et al. 2020

Preprint

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Background Microvesicles (MVs) are submicron membrane vesicles as mediators of intercellular communication. The aim of our study was to investigate protective mechanism of circulating MVs derived from ischemic preconditioning (IPC-MVs) on myocardial I/R injury. Results Administration of IPC-MVs reduced infarct size and activity of lactate dehydrogenase (LDH) in myocardial I/R injury in vivo. Meanwhile, IPC-MVs could increase cell viability and reduce LDH activity in hypoxia/reoxygenation (H/R) injured H9c2 cells in vitro. Microarray analysis demonstrated that miR-133a-3p expression in IPC-MVs increased apparently compared with Sham-MVs. We found that miR-133a-3p increased cell viability, decreased LDH activity and apoptosis , as well as suppressed H/R-induced endoplasmic reticulum stress (ERS). MVs induced by hypoxic preconditioning enriched with FAM-miR-133a-3p allowed the transfer of miR-133a-3p to target cells. In addition, miR-133a-3p was significantly increased in H/R injured H9c2 cells by treatment with IPC-MVs. Epidermal growth factor receptor (EGFR) is a target gene of miR-133a-3p. AG1478 (EGFR inhibitor) significantly increased cell viability, decreased LDH activity and ERS-induced apoptosis in H9c2 cells under H/R injury. Conclusions The findings of this study showed that IPC-MVs exerted cardioprotective effects by transferring miR-133a-3p into H/R injured cardiomyocytes targeting EGFR, thus attenuating ERS-induced apoptosis. MiR-133a-3p transferred by IPC-MVs may provide a novel therapy for myocardial I/R injury.

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Section: Discussionsupporting

confidence: 44%

Section: Introductionmentioning

confidence: 88%

Section: Establishment Of the I/r And Ipc Model In Vivomentioning

confidence: 99%

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MiR-133a-3p transferred by circulating microvesicles derived from myocardial ischemic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury

Zhao

Zhu

Shang

et al. 2020

Preprint

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“…MSC-derived MVs were able to face the detrimental effects of ischemia and reperfusion (I/R) injury in the kidney ( 266 ). Similarly, MVs derived from myocardial ischemia could protect hearts from I/R injury in rats through calcium regulatory proteins to alleviate intrinsic myocardial mitochondrial and endoplasmic reticulum apoptotic pathways ( 267 ). Interestingly, the effect of cardiosphere-derived cells (CDC) on the therapeutic regeneration of the infarcted myocardium shown in a clinical trial ( 268 ) seems to be mediated by CDC-derived extracellular vesicles ( 269 ).…”

Section: Pharmacological and Non-pharmacological Interventionmentioning

confidence: 99%

Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse

Badimon¹,

Suades²,

Arderiu³

et al. 2017

Front. Cardiovasc. Med.

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Atherosclerosis (AT) is a progressive chronic disease involving lipid accumulation, fibrosis, and inflammation in medium and large-sized arteries, and it is the main cause of cardiovascular disease (CVD). AT is caused by dyslipidemia and mediated by both innate and adaptive immune responses. Despite lipid-lowering drugs have shown to decrease the risk of cardiovascular events (CVEs), there is a significant burden of AT-related morbidity and mortality. Identification of subjects at increased risk for CVE as well as discovery of novel therapeutic targets for improved treatment strategies are still unmet clinical needs in CVD. Microvesicles (MVs), small extracellular plasma membrane particles shed by activated and apoptotic cells have been widely linked to the development of CVD. MVs from vascular and resident cells by facilitating exchange of biological information between neighboring cells serve as cellular effectors in the bloodstream and play a key role in all stages of disease progression. This article reviews the current knowledge on the role of MVs in AT and CVD. Attention is focused on novel aspects of MV-mediated regulatory mechanisms from endothelial dysfunction, vascular wall inflammation, oxidative stress, and apoptosis to coagulation and thrombosis in the progression and development of atherothrombosis. MV contribution to vascular remodeling is also discussed, with a particular emphasis on the effect of MVs on the crosstalk between endothelial cells and smooth muscle cells, and their role regulating the active process of AT-driven angiogenesis and neovascularization. This review also highlights the latest findings and main challenges on the potential prognostic, diagnostic, and therapeutic value of cell-derived MVs in CVD. In summary, MVs have emerged as new regulators of biological functions in atherothrombosis and might be instrumental in cardiovascular precision medicine; however, significant efforts are still needed to translate into clinics the latest findings on MV regulation and function.

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“…In contrast, recent studies by Ma et al (2015) have shown that transfusion of microvesicles isolated from rats immediately, but not 6 hours after a hind limb ischemia-induced RIPC into recipient rats exposed to heart I/R injury, resulted in an increase in platelet-derived particles in blood associated with reduction in infarct size and improved functional recovery of hearts. The role of IPC-induced circulating microvesicles in cardioprotection against myocardial I/R injury was also confirmed in the study of Wang et al (2016) where authors injected these isolated particles after coronary occlusion-induced IPC to recipient rats that were consequently exposed to MI and found that myocardial infarct size and cardiomyocyte apoptosis as well as LDH release were reduced. In addition, they found a decreased expression of Bax and activity of caspase 3 and increased expression of Bcl-2 and Bcl-2/Bax ratio after IPC-microvesicles treatment suggesting cardioprotective effects of IPC-microvesicles through inhibition of apoptosis induction.…”

Section: Role Of Microvesicles In Ricmentioning

confidence: 74%

Emerging role of non-coding RNAs and extracellular vesicles in cardioprotection by remote ischemic conditioning of the heart

2019

Reviews in Cardiovascular Medicine

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Protective effects of circulating microvesicles derived from myocardial ischemic rats on apoptosis of cardiomyocytes in myocardial ischemia/reperfusion injury

Cited by 11 publications

References 31 publications

MiR-133a-3p transferred by circulating microvesicles derived from myocardial ischemic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury

MiR-133a-3p transferred by circulating microvesicles derived from myocardial ischemic preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury

Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse

Emerging role of non-coding RNAs and extracellular vesicles in cardioprotection by remote ischemic conditioning of the heart

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