scholarly journals Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Chaoxin Jiang ◽  
Qing Zhao ◽  
Chenlong Wang ◽  
Minyan Peng ◽  
Guoqing Hao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cardiac Tissue ◽  
Trinucleotide Repeat ◽  
Cardiac Cells ◽  
Luciferase Reporter ◽  
Myocardial Cells ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Background. Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. Methods. qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells. Results. LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p. Conclusions. LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.

scholarly journals Blockade of LINC01605-enriched exosome generation in M2 macrophages impairs M2 macrophage-induced proliferation, migration, and invasion of human dermal fibroblasts

2021 ◽  
Vol 35 ◽  
pp. 205873842110167
Author(s):  
Zhensen Zhu ◽  
Bo Chen ◽  
Liang Peng ◽  
Songying Gao ◽  
Jingdong Guo ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Dermal Fibroblast ◽  
Dermal Fibroblasts ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Activated M2 macrophages are involved in hypertrophic scar (HS) formation via manipulating the differentiation of fibroblasts to myofibroblasts having the proliferative capacity and biological function. However, the function of exosomes derived from M2 macrophages in HS formation is unclear. Thus, this study aims to investigate the role of exosomes derived by M2 in the formation of HS. To understand the effect of exosomes derived from M2 macrophages on formation of HS, M2 macrophages were co-cultured with human dermal fibroblast (HDF) cells. Cell Counting Kit-8 assay was performed to evaluate HDF proliferation. To evaluate the migration and invasion of HDFs, wound-healing and transwell invasion assays were performed, respectively. To investigate the interaction between LINC01605 and miR-493-3p, a dual-luciferase reporter gene assay was adopted; consequently, an interaction between miR-493-3p and AKT1 was detected. Our results demonstrated that exosomes derived from M2 macrophages promoted the proliferation, migration, and invasion of HDFs. Additionally, we found that long noncoding RNA LINC01605, enriched in exosomes derived from M2 macrophages, promoted fibrosis of HDFs and that GW4869, an inhibitor of exosomes, could revert this effect. Mechanistically, LINC01605 promoted fibrosis of HDFs by directly inhibiting the secretion of miR-493-3p, and miR-493-3p down-regulated the expression of AKT1. Exosomes derived from M2 macrophages promote the proliferation and migration of HDFs by transmitting LINC01605, which may activate the AKT signaling pathway by sponging miR-493-3p. Our results provide a novel approach and basis for further investigation of the function of M2 macrophages in HS formation.

scholarly journals MiR-486 protects against acute myocardial infarction via regulation of PTEN

2021 ◽  
Vol 20 (9) ◽  
pp. 1845-1853
Author(s):  
Qinfeng Han ◽  
Zhong Xu ◽  
Xiaolei Zhang ◽  
Kun Yang ◽  
Zhifei Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Akt Signaling ◽  
Reporter Gene Assay ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Akt Signaling Pathway ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Qrt Pcr ◽  
Gene Assay

Purpose: To investigate the effect of miR-486 on rats with acute myocardial infarction (AMI), and its mechanism of action.Methods: A rat model of AMI was established. They were randomly divided into 4 groups, namely, sham, model, agomiR-486 and antagomiR-486 groups, respectively. Rats in these different groups were treated with agomiR-21 (5 μL, 40 nmol/mL), antagomiR-21 (5 μL, 40 nmol/mL) or agomiR-NC (5 μL, 40 nmol/mL), respectively. Then, key miRNAs were sorted out using gene-chip assay and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. Luciferase reporter gene assay was conducted to determine the interaction between miR-486 and gene of PTEN. After intraperitoneal injection of agomiR-486 and antagomiR-486, hemodynamics was measured to determine the effect of miR-486 on myocardial function of the rats. The effect of miR-486 expression level on the expression of myocardial enzymes in serum, the morphology of myocardial tissues, and the apoptosis of myocardial tissues in rats, were investigated. Additionally, the effect of miR-486 expression level on PTEN/AKT signaling pathway in the rats was determined by Western blotting.Results: The results of gene-chip and qRT-PCR assays revealed that there were 8 differentially expressed genes in rat myocardial tissues in the model group when compared with the sham group. MiR-486 improved the cardiac function of rats and the morphology of myocardial tissues, but reduced AMI-induced apoptosis of myocardial cells and the expression of myocardial enzymes (markers of myocardial injury) in a dose-dependent manner (p < 0.05). The results of luciferase reporter gene assay showed that PTEN was a direct target of miR-486. In rat models of AMI, a raised expression of miR-486 remarkably suppressed the protein expression level of PTEN and up-regulated that of p-AKT/AKT (p < 0.05).Conclusion: MiR-486 protects against AMI in rats probably by targeting PTEN and activating the AKT signaling pathway. The results of the current study may provide new insights for the treatment of AMI.

scholarly journals Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Kai Liu ◽  
Wen Huang ◽  
Dan-Qing Yan ◽  
Qing Luo ◽  
Xiang Min
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Gene Assay ◽  
Long Intergenic Noncoding Rna ◽  
And Migration

The study evaluated the ability of long intergenic noncoding RNA LINC00312 (LINC00312) to influence the proliferation, invasion, and migration of thyroid cancer (TC) cells by regulating miRNA-197-3p. TC tissues and adjacent normal tissues were collected from 211 TC patients. K1 (papillary TC), SW579 (squamous TC), and 8505C (anaplastic TC) cell lines were assigned into a blank, negative control (NC), LINC00312 overexpression, miR-197-3p inhibitors, and LINC00312 overexpression + miR-197-3p mimics group. The expression of LINC00312, miR-197-3p, and p120 were measured using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed via CCK8 assay, cell invasion through the scratch test, and cell migration via Transwell assay. In comparison with adjacent normal tissues, the expression of LINC00312 is down-regulated and the expression of miR-197-3p is up-regulated in TC tissues. The dual luciferase reporter gene assay confirmed that P120 is a target of miR-197-3p. The expression of LINC00312 and p120 was higher in the LINC00312 overexpression group than in the blank and NV groups. However, the expression of miR-197-3p was lower in the LINC00312 overexpression group than in the blank and NC groups. The miR-197-3p inhibitors group had a higher expression of miR-197-3p, but a lower expression of p120 than the blank and NC groups. The LINC00312 overexpression and miR-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and NC groups. These results indicate that a LINC00312 overexpression inhibits the proliferation, invasion, and migration of TC cells and that this can be achieved by down-regulating miR-197-3p.

scholarly journals CircRNA1615 Inhibits Ferroptosis via Modulation of Autophagy by the miRNA152-3p/LRP6 Axis in Cardiomyocytes of Myocardial Infarction

2021 ◽  
Author(s):  
Rui-lin Li ◽  
Cheng-hui Fan ◽  
Shi-yu Gong ◽  
Sheng Kang
Keyword(s):  
Myocardial Infarction ◽  
Molecular Mechanism ◽  
Biological Function ◽  
Myocardial Cell ◽  
Pathological Process ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Abstract Background Searching for new molecular targets of ferroptosis is gradually becoming the focus in the field of cardiovascular disease research. This study was aimed to explore the biological function and molecular mechanism of ferroptosis of circRNA modulation in cardiomyocytes of myocardial infarction (MI).Method We explored the regulatory effect and molecular mechanism of LPR6 on myocardial cell ferroptosis by establishing a model of MI in vivo and in vitro, constructed the regulatory network of circRNA-miRNA-LRP6 by the bioinformatics analysis, and focused on the biological function and molecular mechanism of circRNA1615 regulating ferroptosis in MI by the overexpression or knockdown of circRNA1615, the RIP experiments, and double luciferase reporter gene assay.Results Ferrostatin-1(ferroptosis inhibitor) can improve the pathological process of MI; LRP6 was involved in the process of ferroptosis in cardiomyocytes; LRP6 deletion regulates ferroptosis in cardiomyocytes through autophagy; Screening and identification of circRNA1615 targets LRP6; circRNA1615 inhibits ferroptosis in cardiomyocytes; circRNA1615 regulates the expression of LRP6 through sponge adsorption of miR-152-3p, and then prevent LRP6-mediated autophagy-related ferroptosis in cardiomyocytes, finally regulate the pathological process of MI.Conclusions CircRNA1615 inhibits ferroptosis via modulation of autophagy by the miRNA152-3p/LRP6 molecular axis in cardiomyocytes of myocardial infarction.

scholarly journals Down-regulation of lncRNA UCA1 enhances radiosensitivity in prostate cancer by suppressing EIF4G1 expression via sponging miR-331-3p

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Minhua Hu ◽  
Jincheng Yang
Keyword(s):  
Prostate Cancer ◽  
Noncoding Rna ◽  
Underlying Mechanism ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Western Blot Assay ◽  
Eukaryotic Translation ◽  
Gene Assay

Abstract Background We aimed to explore the role of long noncoding RNA urothelial carcinoma-associated 1 (lncRNA UCA1) and its underlying mechanism in the radioresistance of prostate cancer (PCa). Methods QRT-PCR was conducted to measure the expression of UCA1, microRNA-331-3p (miR-331-3p) and eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) in PCa tissues and cells. The relative protein level was determined by western blot assay. Cell proliferation and apoptosis were detected by MTT, colony formation assay, and flow cytometry, respectively. The target interaction between miR-331-3p and UCA1 or EIF4G1 was predicted through bioinformatics analysis, and verified by dual-luciferase reporter gene assay system. Results The high levels of UCA1 and EIF4G1 as well as the low level of miR-331-3p were observed in PCa tissues and cell lines. UCA1 and EIF4G1 expression were significantly upregulated by Gy radiation treatement. UCA1 or EIF4G1 knockdown repressed cell growth and enhanced cell apoptosis in 22RV1 and DU145 cells under radiation. Moreover, overexpression of EIF4G1 abolished UCA1 knockdown-induced effect on 6 Gy irradiated PCa cells. UCA1 sponged miR-331-3p to regulate EIF4G1 expression. Conclusions LncRNA UCA1 deletion suppressed the radioresistance to PCa by suppressing EIF4G1 expression via miR-331-3p. UCA1 acted as a potential regulator of radioresistance of PCa, providing a promising therapeutic target for PCa.

scholarly journals Long noncoding RNA H19 accelerates tenogenic differentiation by modulating miR-140-5p/VEGFA signaling

2021 ◽  
Vol 65 (3) ◽  
Author(s):  
You-Jie Liu ◽  
Hua-Jun Wang ◽  
Zhao-Wen Xue ◽  
Lek-Hang Cheang ◽  
Man-Seng Tam ◽  
...  
Keyword(s):  
Stem Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Tendon Healing ◽  
Tendon Injury ◽  
Clinical Treatment ◽  
Luciferase Reporter ◽  
Cuff Tear ◽  
Tenogenic Differentiation ◽  
Gene Assay

Rotator cuff tear (RCT) is a common tendon injury, but the mechanisms of tendon healing remain incompletely understood. Elucidating the molecular mechanisms of tenogenic differentiation is essential to develop novel therapeutic strategies in clinical treatment of RCT. The long noncoding RNA H19 plays a regulatory role in tenogenic differentiation and tendon healing, but its detailed mechanism of action remains unknown. To elucidate the role of H19 in tenogenic differentiation and tendon healing, tendon-derived stem cells were harvested from the Achilles tendons of Sprague Dawley rats and a rat model of cuff tear was established for the exploration of the function of H19 in promoting tenogenic differentiation. The results showed that H19 overexpression promoted, while H19 silencing suppressed, tenogenic differentiation of tendon-derived stem cells (TDSCs). Furthermore, bioinformatic analyses and a luciferase reporter gene assay showed that H19 directly targeted and inhibited miR-140-5p to promote tenogenic differentiation. Further, inhibiting miR-140-5p directly increased VEGFA expression, revealing a novel regulatory axis between H19, miR-140-5p, and VEGFA in modulating tenogenic differentiation. In rats with RTC, implantation of H19-overexpressing TDSCs at the lesion promoted tendon healing and functional recovery. In general, the data suggest that H19 promotes tenogenic differentiation and tendon-bone healing by targeting miR-140-5p and increasing VEGFA levels. Modulation of the H19/miR-140-5p/VEGFA axis in TDSCs is a new potential strategy for clinical treatment of tendon injury.

The Oncogenic Capacities of Long Noncoding RNA SNHG1 in Bladder Cancer by inducing proliferation and repressing apoptosis via upregulation of microRNA-9-3p-targeted MDM2

2021 ◽  
Author(s):  
Weizhang Xu ◽  
Yun Hu ◽  
Haifei Xu ◽  
Haofeng Liu ◽  
Xiaolin Wang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cell ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Bladder Cancer Cell ◽  
Luciferase Reporter ◽  
Mechanistic Investigation ◽  
Gene Assay ◽  
Cancer Tissues

Abstract Background The involvement of long noncoding RNA small nucleolar RNA host gene 1 (lncRNA SNHG1) was documented in numerous cancers, including bladder, pancreatic and prostate cancers. However, the further mechanistic investigation of SNHG1 in bladder is still needed to conduct. With this purpose, tissue, cell, and animal experiments were implemented in our research to figure out the specific mechanism of SNHG1 in bladder cancer via microRNA-9-3p (miR-9-3p). Methods In harvested bladder cancer tissues, RNA-FISH and RT-qPCR were adopted for SNHG1 expression measurement and RT-qPCR for miR-9-3p expression determination. The impacts of SNHG1, miR-9-3p, MDM2, and PPARγ on cell viability, proliferation, and apoptosis were evaluated by gain- and loss-of-function approaches. RT-qPCR and western blot analysis were performed to detect expression of MDM2, PPARγ, and apoptosis-related factors. RNA pull-down, RIP, dual luciferase reporter gene assay, and IP experiment were utilized to assess the modulatory relationship among SNHG1, miR-9-3p, MDM2, and PPARγ. Tumorigenic ability of bladder cancer cells was measured in vivo. Results High SNHG1 and poor miR-9-3p expression was identified in bladder cancer tissues and cells. Mechanistically, SNHG1 bound to miR-9-3p which negatively targeted MDM2. MDM2 augmented PPARγ ubiquitination to downregulate PPARγ. Bladder cancer cell proliferation was diminished and cell apoptosis was enhanced by silencing SNHG1 or MDM2 or overexpressing miR-9-3p. Similarly, SNHG1 silencing orchestrated miR-9-3p/MDM2/PPARγ axis to depress bladder cancer cell tumorigenesis in vivo. Conclusion In summary, the obtained data provided the novel insight of the anti-oncogenic mechanism of silencing SNHG1 in bladder cancer by activating PPARγ via downregulation of miR-9-3p-targeted MDM2.

scholarly journals Tumor Inhibitory Effect of Long Non-coding RNA LOC100505817 on Gastric Cancer

2021 ◽  
Vol 27 ◽  
Author(s):  
Lei Zheng ◽  
Liying Kang ◽  
Yan Cheng ◽  
Junli Cao ◽  
Lijie Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Gastric cancer (GC) is one of the major malignancies worldwide. Emerging evidence has revealed the potential involvement of long noncoding RNA (lncRNA) in human genetic disorders and cancer, but the role of LOC100505817 remains unknown. Thus, in this study, we isolated tissues from GC patients to characterize the functional importance of LOC100505817 in GC tumorigenesis. We also proposed a hypothesis that the regulation of Wnt/β-catenin pathway by LOC100505817 was regulated by miR-20a-mediated WT1. After the collection of cancer tissues and adjacent tissues were obtained from GC patients, expression of LOC100505817, Wnt/β-catenin pathway- and EMT-related genes was quantified. Ectopic expression and knockdown experiments were applied in order to investigate the protective role of LOC100505817 in the progression of GC. Subsequently, cell viability, flow cytometry for apoptosis and cell cycle were detected via CCK-8, while migration and invasion were determined using scratch test and Transwell assay respectively. Then interactions among LOC100505817, miR-20a and WT1 were explored by dual luciferase reporter gene assay, RNA pull down assay and RNA binding protein immunoprecipitation (RIP) assay. The results found poor expression LOC100505817 was poorly expressed in GC cells and tissues. Overexpressed LOC100505817 resulted in the significant reduction of cell proliferation, migration and invasion as well as the expression of Wnt2b, β-catenin, CyclinD1, N-cadherin, Vimentin and snail, while increased cell apoptosis along with the expression of E-cadherin. Wnt/β-catenin pathway and EMT in GC cells were suppressed by LOC100505817 through miR-20a-inhibted WT1. In summary, our results provided evidence suggesting that LOC100505817 inhibits GC through LOC100505817-mediated inhibition of Wnt/β-catenin pathway, that leads to the overall restraining of GC cell proliferation, migration and invasion through miR-20a-reduced WT1.

scholarly journals Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

2020 ◽  
Author(s):  
Xiaomin Hu ◽  
Bojiang Liu ◽  
Peng Wu ◽  
Yuheng Lang ◽  
Tong Li
Keyword(s):  
Myocardial Infarction ◽  
Hydrogen Sulfide ◽  
Cardiac Function ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Luciferase Reporter ◽  
H9c2 Cardiomyocytes

Abstract Background: Ischemia/Reperfusion (I/R) Injury largely limits the efficacy of revascularization in acute myocardial infarction. Long noncoding RNA (lncRNA) Oprm1 is protective in cerebral I/R injury. However, the effect of lncRNA Oprm1 on myocardial I/R injury and its mechanism remains unknown.Methods: We ligated and then released the left anterior descending coronary artery of adult male rats to build the I/R model in vivo, while an H9c2 cardiomyocytes hypoxia-reoxygenation (H/R) model was also used. Myocardial infarction area, cardiac function, histology, Tunnel staining, cell viability, and vital protein expression was conducted and compared.Results: lncRNA Oprm1 was significantly down-regulated in the I/R injury model. When administered with the AAV9-Oprm1 vector, the myocardial injury and cardiac function were mitigated and preserved, with apoptosis reduced. The cystathionine-γ-lyase (CSE) expression and hydrogen sulfide (H2S) expression were increased. The dual-luciferase reporter gene revealed the targeted relationship between lncRNA Oprm1 and miR-30b-5p. In H9c2 cardiomyocytes models, the miR-30b-5p blocked the protective effect of lncRNA Oprm1 on H/R injury, when Bcl-2, Bcl-xl was down-regulated, and HIF-1α, Bnip-3, Caspase-3, and Caspase-9 up-regulated.Conclusions: lncRNA Oprm1can competitively combines with miR-30b-5p, which down-regulates the expression of CSE. When administered with lncRNA Oprm1, increased endogenous H2S can reduce apoptosis and protect the myocardium from I/R injury via activating PI3K/Akt pathway and inhibiting HIF1-α activity.

Extracellular Vesicles Enriched with miR-150 Released by Macrophages Regulates the TP53-IGF-1 Axis to Alleviate Myocardial Infarction

2020 ◽  
Author(s):  
Suxia Zheng ◽  
Maolei Gong ◽  
Jing Chen
Keyword(s):  
Myocardial Infarction ◽  
Extracellular Vesicles ◽  
Caspase 3 ◽  
Luciferase Reporter ◽  
Tunel Staining ◽  
Loss Of Function ◽  
Luciferase Reporter Gene ◽  
Inflammatory Infiltration ◽  
Gene Assay

Myocardial infarction (MI) is recognized as a major cause of death and disability around the world. Macrophage-derived extracellular vesicles (EVs) have been reportedly involved in the regulation of cellular responses to MI. Thus, we sought to clarify the mechanism by which macrophage-derived EVs regulate this process. RT-qPCR was carried out to determine miR-150 expression in an MI mouse model with ligation of the left anterior descending coronary artery (LAD) and in hypoxia/reoxygenation (H/R)-exposed cardiomyocytes. Bioinformatics analysis and dual luciferase reporter gene assay were adopted to identify the correlation of miR-150 with TP53 expression in cardiomyocytes. Gain- and loss-of function experiments were conducted in H/R-induced cardiomyocytes, cardiomyocytes incubated with EVs from miR-150 mimic-transfected macrophages, or MI-model mice treated with EVs from miR-150 mimic-transfected macrophages. HE and TUNEL staining assays were used for detecting inflammatory infiltration and cell apoptosis. The release of LDH by dead cardiomyocytes was measured with an LDH kit, and the apoptosis-related proteins, Bax, and cleaved-caspase 3 were determined by Western blot analysis. miR-150 expression was downregulated in the infarcted cardiac tissues of MI mice. Macrophage-derived EVs could transfer miR-150 into cardiomyocytes, where it directly targeted and suppressed TP53. Furthermore, miR-150 suppressed PTEN and activated p-AKT to upregulate IGF-1 expression. Furthermore, increased expression of EV-derived miR-150 prevented cardiomyocyte apoptosis in vitro, as evidenced by downregulated Bax and cleaved-caspase 3 and upregulated Bcl2 and alleviated MI in vivo. In conclusion, our study demonstrates the cardioprotective effect of macrophage-derived EV-miR-150 on MI-induced heart injury through negatively regulating the TP53-IGF-1 signaling pathway.

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