microRNA-423-3p exosomes derived from cardiac fibroblasts mediates the cardioprotective effects of ischaemic post-conditioning

Luo, Hongyu; Li, Xiaohui; Li, Tangzhiming; Zhao, Lin; He, Jingsong; Zha, Lihuang; Qi, Qiangqiang; Yu, Zaixin

doi:10.1093/cvr/cvy231

Cited by 88 publications

(63 citation statements)

References 43 publications

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“…Accumulating recent evidences reported that microRNA-449, microRNA-423, microRNA-204, and microRNA-665 concentrations were critically altered during H/R-induced cardiomyocyte cell injury. However, H/R-induced H9c2 cells treated with specific inhibition or mimic-miRNAs significantly regulated various cellular inflammatory pathways through their target genes (notch-1, RAP2C, SIRT1, AK1, and Cnr2, respectively) and dramatically reduced oxidative stress, caspase-3 activity, apoptosis, and amazingly protects cardiomyocyte cell injury with obviously increased cellular viability [10,11,25,26]. Very recently, Liang et al research group demonstrated that microRNA-181c-5p expressions were significantly upregulated in hypoxic reoxygentaion-exposed H9c2 cardiomyocytes and rat myocardial ischemia-reperfusion injury (I-RI).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-375 Protects Cardiomyocyte Injury following Hypoxic-Reoxygenation Injury

Sheikh

2020

Oxidative Medicine and Cellular Longevity

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The aim of the study was to evaluate the clinical significance of microRNA-375 in acute myocardial infarction patients and its mimic action in hypoxia/reoxygenation- (H/R-) induced ventricular cardiomyocyte H9c2 injury. In the current study, 90 ST-elevated acute MI patients (STEMI), 75 non-ST-elevated acute MI patients (NSTEMI), 90 healthy subjects, 14 weeks old mice, and ventricular cardiomyocyte H9c2 were included. The expressions of plasma microRNA-375 in patients with STEMI and NSTEMI and AMI mouse models were remarkably decreased than in controls (P<0.001). The areas under the curve (AUC) of plasma microRNA-375 were revealed 0.939 in STEMI and 0.935 in NSTEMI subjects. Moreover, microRNA-375 levels in H/R-exposed cardiac H9c2 cells were evidently downregulated and significantly increased apoptosis rate and caspase-3 activity levels, while overexpression of miR-375 remarkably reduced apoptosis percentage and caspase-3 levels as compared with normal cells. Furthermore, this study also demonstrated that Nemo-like kinase (NLK), NLK mRNA, and protein expression levels were significantly downregulated in H/R-injured H9c2 cells, on the contrary, H9c2 cells transfected with mimic-miR-375 greatly upregulated NLK mRNA and protein expression. Plasma microRNA-375 may serve as an essential clinical biomarker for diagnosis of early-stage AMI. Mimic expression of miR-375 significantly prevented H/R-induced cardiomyocyte injury by decreasing caspase-3 activity through upregulation of the NLK gene, recommended as a new therapeutic option for AMI patient.

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Section: Discussionmentioning

confidence: 99%

Overexpression of miR-375 Protects Cardiomyocyte Injury following Hypoxic-Reoxygenation Injury

Sheikh

2020

Oxidative Medicine and Cellular Longevity

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“…The increased secretion of extracellular vesicles of trophoblastic origin containing miRNAs into the maternal blood flow due to placental dysfunction in PE can contribute to systemic biological changes. Among the miRNAs circulating in blood plasma, we identified (let-7g-5p, miR-26a-5p, miR-28 (-28-3p, -151a-3p), -30a-5p, -148a-3p, -181 (-181a-5p), -183-5p, -186-5p, -188 (-532-5p), -192-5p, and -320 (-320a), which change their expression in response to oxygen deprivation [18][19][20], oxidative stress (miR-140-3p, -143-3p, -378a-3p) [46], and are associated with immune and inflammatory responses (miR-375) [47], as well as ischemia/reperfusion (miR-423-3p) [48]. In general, our results are consistent with the data of other authors.…”

Section: Discussionmentioning

confidence: 99%

Preeclampsia: The Interplay between Oxygen-Sensitive miRNAs and Erythropoietin

Gusar

Timofeeva

Chagovets

et al. 2020

JCM

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Changes in the oxygen partial pressure caused by a violation of uteroplacental perfusion are considered a powerful inducer of a cascade of reactions leading to the clinical manifestation of preeclampsia (PE). At the same time, the induction of oxygen-dependent molecule expression, in particular, miRNA and erythropoietin, is modulated. Therefore, the focus of our study was aimed at estimating the miRNA expression profile of placental tissue and blood plasma in pregnant women with preeclampsia using deep sequencing and quantitative RT-PCR, as well as determining the concentration of erythropoietin. The expression of miR-27b-3p, miR-92b-3p, miR-125b-5p, miR-181a-5p, and miR-186-5p, as regulated by hypoxia/reoxygenation, was significantly increased in blood plasma during early-onset preeclampsia. The possibility of detecting early PE according to the logistic regression model (miR-92b-3p, miR-125b-5p, and miR-181a-5p (AUC = 0.91)) was evaluated. Furthermore, the erythropoietin level, which is regulated by miR-125b-5p, was significantly increased. According to PANTHER14.1, the participation of these miRNAs in the regulation of pathways, such as the hypoxia’s response via HIF activation, oxidative stress response, angiogenesis, and the VEGF signaling pathway, were determined.

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“…As a kind of paracrine factor, MVs allow the transfer of cytoplasmic components such as proteins, mRNAs and miRNAs from one cell to another [8]. However, circulating MVs vary in their components, which varies with the different parent cell types or different stimuli, thus playing different biological roles in occurrence and development of diseases [9,12]. Recent studies have revealed that functional miRNAs can be transferred by MVs and appear to specially home to the site of injury within infarcted myocardium, and MVs were considered as major vector of circulating miRNAs [10].…”

Section: Discussionmentioning

confidence: 99%

“…Multiple experiments have shown that MVs derived from various cell types could play intercellular communication role in diagnostic and therapeutic effects of cardiovascular diseases, mainly by delivering proteins, cytokines and gene messages such as mRNAs and microRNAs (miRNAs) to target cells [8]. Among the components of MVs, miRNAs have been shown to play important roles that regulate the pathophysiological consequences of myocardial I/R injury [9], which can be released from various cells by MVs that protect them from degradation and guarantee their stability and circulation through the blood stream [10], suggesting miRNA in MVs could be a potent therapeutic target and tool for protecting myocardium against I/R injury.…”

Section: Introductionmentioning

confidence: 99%

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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microRNA-423-3p exosomes derived from cardiac fibroblasts mediates the cardioprotective effects of ischaemic post-conditioning

Cited by 88 publications

References 43 publications

Overexpression of miR-375 Protects Cardiomyocyte Injury following Hypoxic-Reoxygenation Injury

Overexpression of miR-375 Protects Cardiomyocyte Injury following Hypoxic-Reoxygenation Injury

Preeclampsia: The Interplay between Oxygen-Sensitive miRNAs and Erythropoietin

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

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