M2 macrophage-derived exosomes carry microRNA-148a to alleviate myocardial ischemia/reperfusion injury via inhibiting TXNIP and the TLR4/NF-κB/NLRP3 inflammasome signaling pathway

Dai, Yuxiang; Shen, Wei; Chang, Shufu; Ren, Daoyuan; Shali, Shalaimaiti; Li, Chenguang; Yang, Hongbo; Huang, Zheyong; Ge, Junbo

doi:10.1016/j.yjmcc.2020.02.007

Cited by 167 publications

(161 citation statements)

References 49 publications

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“…Some reliable evidence demonstrated that M2 macrophage improves tissues injury through secreting exosomes carrying miRNA. For instance, M2 macrophage was proved to attenuate ischemia/reperfusion‐induced injury in myocardial via deriving exosomal miR‐148 24 . Here, we successfully induced podocytes injury using HG, and proofed that M2 macrophage could notably ameliorate HG‐induced podocytes injury via secreting exosomes.…”

Section: Discussionmentioning

confidence: 58%

“…For instance, M2 macrophage was proved to attenuate ischemia/reperfusioninduced injury in myocardial via deriving exosomal miR-148. 24 Here, we successfully induced podocytes injury using HG, and proofed that M2 macrophage could notably ameliorate HG-induced podocytes injury via secreting exosomes. We further indicated that miR-25-3p was increased in M2 macrophage-derived exosomes.…”

Section: Discussionmentioning

confidence: 62%

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M2 macrophage‐derived exosomal miR‐25‐3p improves high glucose‐induced podocytes injury through activation autophagy via inhibiting DUSP1 expression

et al. 2020

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Diabetic nephropathy (DN) is the primary reason of chronic kidney disease. The aim of our study is to explore the role and action mechanism of M2 macrophage-derived exosomes in high glucose (HG)-induced podocytes injury. Here, 30 mmol/L of HG was used to induce podocytes injury. Annexin V-FITC/ PI double staining was performed to measure podocytes apoptosis, and western blot was carried out to ensure proteins expression. The shape of exosomes was identified using TEM. Besides, the expression of miR-25-3p was determined by qRT-PCR, FAM-labeled miR-25-5p combined with DiI-labeled exosomes were utilized to explore the uptake of podocytes to exosomes. Relationship between miR-25-3p and DUSP family members was ensued by luciferase activity assay. In the beginning, we found that M2 macrophage ameliorated HGinduced podocytes apoptosis and epithelial-mesenchymal transition through secreting exosomes. Subsequently, highly expressed miR-25-3p was found in M2 macrophage-derived exosomes that effectively improved HG-induced podocytes injury. Furthermore, inhibition of miR-25-3p in M2 macrophage inefficiently repressed HG-induced podocytes injury, thus we proposed that M2 macrophage attenuated podocytes injury through secreting exosomal miR-25-3p. Then, we used an autophagy inhibitor to stimulate podocytes, and demonstrated that M2 macrophage-derived exosomal miR-25-3p improved HGinduced podocytes injury through activating autophagy. Finally, DUSP1 was proved to be a downstream target and mediated the inhibition of exosomal miR-25-3p to HG-induced podocytes injury. Our results indicated that M2 macrophage could improve HG-induced podocytes injury via secreting exosomal miR-25-3p to activate autophagy of the cells through suppressing DUSP1 expression. We proved a newly potential therapy strategy for DN treatment.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 62%

M2 macrophage‐derived exosomal miR‐25‐3p improves high glucose‐induced podocytes injury through activation autophagy via inhibiting DUSP1 expression

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“…Pyroptosis is a pro-inflammatory cell death program that occurs in response to the release of damage-associated molecular patterns (DAMPs) such as mitochondrial DNA [30] which results in the assembly of the intracellular NLRP3 inflammasome complex, and contributes to acute myocardial IRI [31] . Inhibition of the NLRP3 inflammasome by pharmacological agents, genetic ablation, and M2 macrophage-derived exosomes, has been shown to reduce MI size in small animal MI models [ 32 , 33 ]. Ferroptosis is a regulated cell death program that occurs in response to accumulation of iron-dependent lipid peroxidation that occurs in response to acute myocardial IRI due to mitochondrial accumulation of iron and oxidative stress, providing a novel mitochondrial target for cardioprotection following AMI [34] .…”

Section: Targeting the Mitochondrial Permeability Transition Pore Formentioning

confidence: 99%

Mitochondria in acute myocardial infarction and cardioprotection

et al. 2020

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Acute myocardial infarction (AMI) and the heart failure (HF) that often follows are among the leading causes of death and disability worldwide. As such, new treatments are needed to protect the myocardium against the damaging effects of the acute ischaemia and reperfusion injury (IRI) that occurs in AMI, in order to reduce myocardial infarct (MI) size, preserve cardiac function, and improve patient outcomes. In this regard, cardiac mitochondria play a dual role as arbiters of cell survival and death following AMI. Therefore, preventing mitochondrial dysfunction induced by acute myocardial IRI is an important therapeutic strategy for cardioprotection. In this article, we review the role of mitochondria as key determinants of acute myocardial IRI, and we highlight their roles as therapeutic targets for reducing MI size and preventing HF following AMI. In addition, we discuss the challenges in translating mitoprotective strategies into the clinical setting for improving outcomes in AMI patients.

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“…For example, myocardial ischemia/reperfusion (I/R) injury is characterized by irreversible injury to the myocardium and results in heart dysfunction. Interestingly, EVs from M2-like macrophages deliver miR-148a to mitigate I/R-induced myocardial injury via suppressing the overloaded Ca 2+ and inflammatory cytokine production in cardiomyocytes 111 . The anti-inflammatory effect of Mφ-EVs was also investigated in the models of diabetic wound, which is characterized by a persistent inflammatory response.…”

Section: Therapeutic Roles Of Mφ-evs In Diseasesmentioning

confidence: 99%

Macrophage-derived extracellular vesicles: diverse mediators of pathology and therapeutics in multiple diseases

et al. 2020

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Macrophages (Mφ) are primary innate immune cells that exhibit diverse functions in response to different pathogens or stimuli, and they are extensively involved in the pathology of various diseases. Extracellular vesicles (EVs) are small vesicles released by live cells. As vital messengers, macrophage-derived EVs (Mφ-EVs) can transfer multiple types of bioactive molecules from macrophages to recipient cells, modulating the biological function of recipient cells. In recent years, Mφ-EVs have emerged as vital mediators not only in the pathology of multiple diseases such as inflammatory diseases, fibrosis and cancers, but also as mediators of beneficial effects in immunoregulation, cancer therapy, infectious defense, and tissue repair. Although many investigations have been performed to explore the diverse functions of Mφ-EVs in disease pathology and intervention, few studies have comprehensively summarized their detailed biological roles as currently understood. In this review, we briefly introduced an overview of macrophage and EV biology, and primarily focusing on current findings and future perspectives with respect to the pathological and therapeutic effects of Mφ-EVs in various diseases.

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M2 macrophage-derived exosomes carry microRNA-148a to alleviate myocardial ischemia/reperfusion injury via inhibiting TXNIP and the TLR4/NF-κB/NLRP3 inflammasome signaling pathway

Cited by 167 publications

References 49 publications

M2 macrophage‐derived exosomal miR‐25‐3p improves high glucose‐induced podocytes injury through activation autophagy via inhibiting DUSP1 expression

M2 macrophage‐derived exosomal miR‐25‐3p improves high glucose‐induced podocytes injury through activation autophagy via inhibiting DUSP1 expression

Mitochondria in acute myocardial infarction and cardioprotection

Macrophage-derived extracellular vesicles: diverse mediators of pathology and therapeutics in multiple diseases

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