Effect of intravenous transplantation of hUCB-MSCs on M1/M2 subtype conversion in monocyte/macrophages of AMI mice

Peng, Yi; Chen, Bingquan; Zhao, Ji-Ling; Peng, Zhiyong; Xu, Weifang; Yu, Guopan

doi:10.1016/j.biopha.2018.12.095

Cited by 27 publications

(13 citation statements)

References 35 publications

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“…Consequently, protecting cardiomyocytes against ischemic injury serves as a vital strategy for the treatment of acute myocardial infarction. Furthermore, the infiltration of inflammatory cells such as macrophages and neutrophils has been observed in the border areas on the occurrence of acute myocardial infarction, indicating that suppression of inflammatory reaction in cardiac ischemic regions also provides a potential and effective pathway (Crea and Libby, 2017; Loyer et al., 2018; Ong et al., 2018; Zhang et al., 2018a; Peng et al., 2019). So far, although increasing knowledge has been gained on acute myocardial infarction and various kinds of interventions have been developed, the gross mortality of acute myocardial infarction patients remains high, and more effective therapeutic strategies are still demanded.…”

Section: Introductionmentioning

confidence: 99%

The Role of Autophagy in Acute Myocardial Infarction

Wu¹,

Zhang²,

2019

Front. Pharmacol.

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Acute myocardial infarction refers to a sudden death of cardiomyocytes, which leads to a large mortality worldwide. To attenuate acute myocardial infarction, strategies should be made to increase cardiomyocyte survival, improve postinfarcted cardiac function, and reverse the process of cardiac remodeling. Autophagy, a pivotal cellular response, has been widely studied and is known to be involved in various kinds of diseases. In the recent few years, the role of autophagy in diseases has been drawn increasing attention to by researchers. Here in this review, we mainly focus on the discussion of the effect of autophagy on the pathogenesis and progression of acute myocardial infarction under ischemic and ischemia/reperfusion injuries. Furthermore, several popular therapeutic agents and strategies taking advantage of autophagy will be described.

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Section: Introductionmentioning

confidence: 99%

The Role of Autophagy in Acute Myocardial Infarction

Wu¹,

Zhang²,

2019

Front. Pharmacol.

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“…Pathologically, MI is characterized by myocardial cell death 1 and pro-inflammatory responses 3,4 , which further exacerbate cardiac injury. MSCs, on the other hand, have been demonstrated to exert anti-apoptotic, regenerative and anti-inflammatory effects in animal models of MI [5][6][7][8][9] . Furthermore, a recent meta-analysis with data from 14 randomized placebo-controlled trials suggested that MSC therapy is safe and beneficial in terms of the improved left ventricular ejection fraction and regenerative outcomes 6 .…”

Section: Introductionmentioning

confidence: 99%

Exosomal miR-25-3p from mesenchymal stem cells alleviates myocardial infarction by targeting pro-apoptotic proteins and EZH2

et al. 2020

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Mesenchymal stem cell (MSC) therapy is a promising approach against myocardial infarction (MI). Studies have demonstrated that MSCs can communicate with other cells by secreting exosomes. In the present study, we aimed to identify exosomal microRNAs that might contribute to MSC-mediated cardioprotective effects. Primary cardiomyocytes were deprived of oxygen and glucose to mimic MI in vitro. For the animal model of MI, the left anterior descending artery was ligated for 1 h, followed by reperfusion for 12 h. MSC-derived exosomes were used to treat primary cardiomyocytes or mice. Cardioprotection-related microRNAs were determined, followed by target gene identification and functional studies with quantitative PCR, western blotting, MTT assay, flow cytometry assay, chromatin immunoprecipitation and dual-luciferase assay. We found that MSC co-culture reduced OGD-induced cardiomyocyte apoptosis and inflammatory responses. Cardioprotection was also observed upon treatment with MSC-derived exosomes in vitro and in vivo. In line with this, exosome uptake led to a significant increase in miR-25-3p in cardiomyocytes. Depletion of miR-25-3p in MSCs abolished the protective effects of exosomes. Mechanistically, miR-25-3p directly targeted the pro-apoptotic genes FASL and PTEN and reduced their protein levels. Moreover, miR-25-3p decreased the levels of EZH2 and H3K27me3, leading to derepression of the cardioprotective gene eNOS as well as the anti-inflammatory gene SOCS3. Inhibition of EZH2 or overexpression of miR-25-3p in cardiomyocytes was sufficient to confer cardioprotective effects in vitro and in vivo. We concluded that exosomal miR-25-3p from MSCs alleviated MI by targeting pro-apoptotic proteins and EZH2.

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“…The results show that ASX alleviated inflammation after AMI and promoted damage repair and that the mechanism of this protective effect may be related to ASX-induced macrophage polarization. [ 26 , 27 ] Peng et al [ 28 ] transplanted human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) via the tail vein into a mouse model of AMI. The results demonstrated that intravenous transplantation of hUCB-MSCs could reduce the inflammatory response by stimulating the conversion of intracardiac and extracardiac macrophage subtype from M1 to M2.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin promotes M2 macrophages and attenuates cardiac remodeling after myocardial infarction by suppression inflammation in rats

Pan

Zhang

Cheng

et al. 2020

Chinese Medical Journal

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Background Cardiac remodeling after acute myocardial infarction (AMI) is an important process. The present study aimed to assess the protective effects of astaxanthin (ASX) on cardiac remodeling after AMI. Methods The study was conducted between April and September 2018. To create a rat AMI model, rats were anesthetized, and the left anterior descending coronary artery was ligated. The rats in the ASX group received 10 mg·kg −1 ·day −1 ASX by gavage for 28 days. On the 1st day after AMI, but before ASX administration, six rats from each group were sacrificed to evaluate changes in the heart function and peripheral blood (PB) levels of inflammatory factors. On the 7th day after AMI, eight rats from each group were sacrificed to evaluate the PB levels of inflammatory factors and the M2 macrophage count using both immunofluorescence (IF) and flow cytometry (FC). The remaining rats were observed for 28 days. Cardiac function was examined using echocardiography. The inflammatory factors, namely, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10, were assessed using enzyme-linked immunosorbent assay. The heart weight/body weight (BW), and lung weight (LW)/BW ratios were calculated, and myocardial fibrosis in the form of collagen volume fraction was measured using Masson trichrome staining. Hematoxylin and eosin (H&E) staining was used to determine the myocardial infarct size (MIS), and TdT-mediated dUTP nick-end labeling staining was used to analyze the myocardial apoptosis index. The levels of apoptosis-related protein, type I/III collagen, transforming growth factor β1 (TGF-β1), metalloproteinase 9 (MMP9), and caspase 3 were assessed by Western blotting. Unpaired t -test, one-way analysis of variance, and non-parametric Mann-Whitney test were used to analyze the data. Results On day 1, cardiac function was worse in the ASX group than in the sham group (left ventricular end-systolic diameter [LVID s ]: 0.72 ± 0.08 vs. 0.22 ± 0.06 cm, t = −11.38; left ventricular end-diastolic diameter [LVID d ]: 0.89 ± 0.09 vs. 0.48 ± 0.05 cm, t = −9.42; end-systolic volume [ESV]: 0.80 [0.62, 0.94] vs. 0.04 [0.03, 0.05] mL, Z = −2.89; end-diastolic volume [EDV]: 1.39 [1.03, 1.49] vs. 0.28 [0.22, 0.32] mL, Z = −2.88; ejection fraction [EF]: 0.40 ± 0.04 vs. 0.86 ± 0.05, t = 10.00; left ventricular fractional shortening [FS] rate: 0.19 [0.18, 0.20] %FS vs. 0.51 [0.44, 0.58] %FS, Z = −2.88, all P < 0.01; n ...

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Effect of intravenous transplantation of hUCB-MSCs on M1/M2 subtype conversion in monocyte/macrophages of AMI mice

Cited by 27 publications

References 35 publications

The Role of Autophagy in Acute Myocardial Infarction

The Role of Autophagy in Acute Myocardial Infarction

Exosomal miR-25-3p from mesenchymal stem cells alleviates myocardial infarction by targeting pro-apoptotic proteins and EZH2

Astaxanthin promotes M2 macrophages and attenuates cardiac remodeling after myocardial infarction by suppression inflammation in rats

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