Exosomal miR-301 derived from mesenchymal stem cells protects myocardial infarction by inhibiting myocardial autophagy

Li, Yong; Yang, Rong; Guo, Bingyan; Zhang, Hongbo; Zhang, Hui; Liu, Suyun; Li, Yongjun

doi:10.1016/j.bbrc.2019.04.138

Cited by 58 publications

(30 citation statements)

References 27 publications

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“…2C and D). In line with preceding studies, the present study discovered that mice undergoing MI surgery exhibited decreased LVEF and LVFS, as well as increased LVEDd and LVESd (39,40), suggesting that MI surgery successfully leads to cardiac insufficiency and ventricular dilatation (Fig. 2E).…”

Section: Resultssupporting

confidence: 91%

Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy

Huang

Chen

et al. 2019

Int J Mol Med

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Post-infarction remodeling is accompanied and influenced by perturbations in the mammalian target of rapamycin (mTOR) signaling. Regulated in development and DNA damage response-1 (Redd1) has been reported to be involved in DNA repair and modulation of mTOR activity. However, little is known about the role of Redd1 in the heart. In the present study the potential contribution of Redd1 overex-pression to the chronic phase of heart failure after myocardial infarction (MI) was explored and the mechanisms underlying Redd1 actions were determined. Redd1 was downregulated in the mouse heart subjected to MI surgery. To determine the role of Redd1 in the process of MI, adeno-associated virus 9 mediated overexpression of Redd1 was used to enhance Redd1 content in cardiomyocytes. Redd1 overexpression improved left ventricular dysfunction and reduced the expansion index. Additionally, Redd1 overexpression resulted in suppressed myocardial apoptosis and improved autophagy. Furthermore, the studies revealed that Redd1 overexpression could inhibit the phosphorylation of mTOR and its downstream effectors P70/S6 kinase and 4EBP1. In conclusion, this study demonstrated that Redd1 overexpression protects against the development and persistence of heart failure post MI by reducing apoptosis and enhancing autophagy via the mTOR signaling pathway. The present study clearly demonstrated that Redd1 is a therapeutic target in the development of heart failure after MI.

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Section: Resultssupporting

confidence: 91%

Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy

Huang

Chen

et al. 2019

Int J Mol Med

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“…In contrast, we detected a diminished expression of miR-301 after MI. Li et al [76], studying exosomes secreted by BMSCs, showed that exosomes carrying overexpressed miR-301 could improve cardiac function and reduce MI area in rats with MI. We were not able to detect the change of miR-301 expression after PBMT.…”

Section: Discussionmentioning

confidence: 99%

Photobiomodulation Therapy on Myocardial Infarction in Rats: Transcriptional and Posttranscriptional Implications to Cardiac Remodeling

et al. 2021

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Background and Objectives: Induction of myocardial infarction (MI) in rats by occlusion of the left anterior descending coronary artery is an experimental model used in research to elucidate functional, structural, and molecular modifications associated with ischemic heart disease. Photobiomodulation therapy (PBMT) has become a therapeutic alternative by modulating various biological processes eliciting several effects, including anti-inflammatory and proproliferative actions. The main objective of this work was to evaluate the effect of PBMT in the modulation of transcriptional and post-transcriptional changes that occurred in myocardium signal transduction pathways after MI. Study Design/Materials and Methods: Continuous wave (CW) non-thermal laser parameters were: 660 nm wavelength, power 15 mW, with a total energy of 0.9 J, fluence of 1.15 J/cm 2 , spot size of 0.785 cm 2 , and time of 60 seconds. Using in silico analysis, we selected and then, quantified the expression of messenger RNA (mRNA) of 47 genes of 9 signaling pathways associated with MI (angiogenesis, cell survival, hypertrophy, oxidative stress, apoptosis, extracellular matrix, calcium kinetics, cell metabolism, and inflammation). Messenger RNA expression quantification was performed in myocardial samples by polymerase chain reaction real-time array using TaqMan customized plates. Results: Our results evidenced that MI modified mRNA expression of several well-known biomarkers related to detrimental cardiac activity in almost all signaling pathways analyzed. However, PBMT reverted most of these transcriptional changes. More expressively, PBMT provoked a robust decrease in mRNA expression of molecules that participate in post-MI inflammation and ECM composition, such as IL-6, TNF receptor, TGFb1, and collagen I and III. Global microRNA (miRNA) expression analysis revealed that PBMT decreased miR-221, miR-34c, and miR-93 expressions post-MI, which are related to deleterious effects in cardiac remodeling. Conclusion:Thus, the identification of transcriptional and post-transcriptional changes induced by PBMT may be used to interfere in the molecular dynamics of cardiac remodeling post-MI.

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“…Besides, through transfection, over expression of miR-301 in BMMSCs increases the expression of exosomal miR-301, which significantly reduces the ratio of LC3-II/LC3-I and increases P62 relative expression in the infarcted myocardial tissue. Notably, the ratio of LC3-II/LC3-I increased, and the expression level of P62 decreased when the degree of autophagy was enhanced ( Li Y. et al, 2019 ).…”

Section: Exosomes Reduce Cardiomyocyte Death After Myocardiac Injurymentioning

confidence: 99%

Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion

Iroegbu

Peng³

et al. 2021

Front. Cell Dev. Biol.

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Cardiovascular disease (CVD) is the leading cause of death in the global population, accounting for about one-third of all deaths each year. Notably, with CVDs, myocardial damages result from myocardial infarction (MI) or cardiac arrhythmias caused by interrupted blood flow. Significantly, in the process of MI or myocardial ischemic-reperfusion (I/R) injury, both regulated and non-regulated cell death methods are involved. The critical factor for patients’ prognosis is the infarct area’s size, which determines the myocardial cells’ survival. Cell therapy for MI has been a research hotspot in recent years; however, exosomes secreted by cells have attracted much attention following shortcomings concerning immunogens. Exosomes are extracellular vesicles containing several biologically active substances such as lipids, nucleic acids, and proteins. New evidence suggests that exosomes play a crucial role in regulating cell death after MI as exosomes of various stem cells can participate in the cell damage process after MI. Hence, in the review herein, we focused on introducing various cell-derived exosomes to reduce cell death after MI by regulating the cell death pathway to understand myocardial repair mechanisms better and provide a reference for clinical treatment.

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Exosomal miR-301 derived from mesenchymal stem cells protects myocardial infarction by inhibiting myocardial autophagy

Cited by 58 publications

References 27 publications

Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy

Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy

Photobiomodulation Therapy on Myocardial Infarction in Rats: Transcriptional and Posttranscriptional Implications to Cardiac Remodeling

Cell Death and Exosomes Regulation After Myocardial Infarction and Ischemia-Reperfusion

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