Effects of mir-21 on Cardiac Microvascular Endothelial Cells After Acute Myocardial Infarction in Rats: Role of Phosphatase and Tensin Homolog (PTEN)/Vascular Endothelial Growth Factor (VEGF) Signal Pathway

Yang, Feng Ying; Liu, Wenwei; Yan, Xiaojuan; Zhou, Hanyun; Zhang, Hongshen; Liu, Jianfei; Yu, Miao; Zhu, Xiaoshan; Ma, Kezhong

doi:10.12659/msm.897773

Cited by 50 publications

(37 citation statements)

References 42 publications

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“…The osteogenic differentiation could be regulated by miR-145 through targeting FOXO1 [37]. Moreover, the effects of FOXO1 on cell biological function and inflammatory reaction have been previously reported [38,39]. Therefore, we considered that the regulatory effects of miR-145 on VECs proliferation and migration and inflammation in ACS might be achieved by targeting FOXO1.…”

Section: Discussionmentioning

confidence: 98%

MicroRNA-145 is involved in endothelial cell dysfunction and acts as a promising biomarker of acute coronary syndrome

Sun

2020

Eur J Med Res

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Background: Acute coronary syndrome (ACS) is a serious type of cardiovascular diseases. This study aimed to investigate the expression patterns and clinical value of in ACS patients, and further uncover the function of miR-145 in ACS rats. Methods:Quantitative real-time PCR was used to estimate the expression of miR-145. Diagnostic value of miR-145 was evaluated, and its correlation with endothelial injury marker (vWF and H-FABP) and pro-inflammatory cytokines (IL-6 and TNF-α) was analyzed. Coronary artery ligation was adopted to construct the ACS rat model, and the effects of miR-145 on endothelial injury, inflammation and vascular endothelial cells (VECs) biological function were examined.Results: Downregulated expression of miR-145 was found in the ACS serum samples compared with the healthy controls. The expression of miR-145 was proved to be a diagnostic biomarker and negatively correlated with vWF, H-FABP, IL-6 and TNF-α. The similar serum expression trends of miR-145 in ACS patients were also observed in the ACS rats, and the overexpression of miR-145 could decrease the elevated vWF, H-FABP, IL-6 and TNF-α in the animal model. Moreover, the upregulation of miR-145 in VECs led to promoted proliferation and migration. The bioinformatics prediction data and luciferase report results indicated that FOXO1 was a direct target of miR-145. Conclusions:In conclusion, it was hypothesized that serum decreased expression of miR-145 may serve as a potential diagnostic biomarker in ACS patients. Overexpression of miR-145 may improve the endothelial injury and abnormal inflammation through targeting FOXO1, indicating that miR-145 serves as a candidate therapeutic target of ACS. CW, Lim DS. Comparison of ticagrelor versus prasugrel for inflammation, vascular function, and circulating endothelial progenitor cells in diabetic patients with non-ST-segment elevation acute coronary syndrome requiring coronary stenting: a prospective, randomized, crossover trial. -217 inhibits proliferation, migration, and invasion via targeting AKT3 in thyroid cancer. Biomed Pharmacother. 2017;95:1718-24.

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Section: Discussionmentioning

confidence: 98%

MicroRNA-145 is involved in endothelial cell dysfunction and acts as a promising biomarker of acute coronary syndrome

Sun

2020

Eur J Med Res

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“…A previous study has indicated that cardiac angiogenesis had a close association with heart failure, while interestingly CMECs play a regulatory role in the process of cardiac angiogenesis (Ma et al, ). For example, miR‐21 shows protective effects against CMEC injury through the PTEN/VEGF signaling pathway following acute myocardial infarction (F. Yang et al, ). Additionally, miR‐200a rescues CMECs in the settings of hypoxia‐reoxygenation injury through mediating the protection of thymosin β4 (Y. Li, Zhu, Liu, Du, & Yu, ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐128 confers protection against cardiac microvascular endothelial cell injury in coronary heart disease via negative regulation of IRS1

Yan

Sun

et al. 2019

Journal Cellular Physiology

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Objective Cardiac microvascular endothelial cells (CMECs) play a critical role in the physiological regulation of coronary blood flow and its dysfunction is associated with myocardium ischemic injury. This study was performed to clarify the effect of microRNA‐128 (miR‐128) on the CMEC injury in coronary heart disease (CHD) by binding to insulin receptor substrate 1 (IRS1). Methods The rat CMECs were cultured by explant culture method and identified by CD31 immunofluorescence assay. CMECs were treated with homocysteine (Hcy), which underwent stress of CHD, followed by treatment of miR‐128 mimics/inhibitors or IRS1 siRNA. Expression of miR‐128, IRS1, and vascular endothelial growth factor (VEGF) was determined. The viability, apoptosis, migration ability, and tube formation ability of CMECs were evaluated. The superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS) of CMECs were evaluated, respectively. Results In rat CMECs, miR‐128 was poorly expressed and IRS1 was highly expressed. Notably, miR‐128 targeted and negatively regulated IRS1. Additionally, the treatment with Hcy in CMECs led to reduced viability, migration ability, tube formation, VEGF expression, SOD activity as well as increased cell apoptosis, MDA and ROS levels. The experimental results demonstrated that miR‐128 mimics and IRS1 siRNA in rat CMECs promoted viability, migration ability, tube formation, VEGF expression, SOD activity, while repressing cell apoptosis, MDA and ROS levels. MiR‐128 inhibitors could reverse the tendencies. Conclusion Collectively, our study provides evidence that miR‐128 targeted and negatively regulated IRS1 expression, whereby the functional injury of CMECs induced by Hcy was ameliorated. Furthermore, protection of miR‐128 was stimulated by reducing oxidative stress.

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“…In response to vascular injury, resveratrol attenuates endothelial function during hyperglycemia via activation of proteasome-dependent degradation of PTEN, which in turn increases Akt phosphorylation (36). Furthermore miR-21 exerts protective effects on endothelial injury through the PTEN/VEGF pathway after acute myocardial infarction (37). Thus, PTEN might be involved in the functional regulation of GECs.…”

Section: Discussionmentioning

confidence: 99%

miR‐132‐3p boosts caveolae‐mediated transcellular transport in glioma endothelial cells by targeting PTEN/PI3K/PKB/Src/Cav‐1 signaling pathway

Cai

Zhang

et al. 2018

The FASEB Journal

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Blood-brain tumor barrier (BTB) impedes the transportation of antitumor therapeutic drugs into brain tumors. Its mechanism is still unknown, but learning how to improve the BTB permeability is critical for drug intervention. Recently, microRNAs (miRNAs) have appeared as regulation factors of numerous biologic processes and therapeutic targets of diverse diseases. In this study, we have identified that miR-132-3p is an essential miRNA by increasing the transcellular transport through the BTB. We found that miR-132-3p expression was significantly up-regulated in glioma endothelial cells (GECs). Furthermore we showed that miR132-3p greatly induced the endocytosis of cholera toxin subunit B and FITC-bovine serum albumin and up-regulated the expression of p-PKB, p-Src and Tyr14 phosphorylation of caveolin-1 (p-Cav-1), while phosphatase and tensin homolog deleted on chromosome 10 (PTEN) expression was markedly down-regulated in GECs. Our results identify PTEN as a direct and functional downstream target of miR-132-3p, which is involved in the regulation of p-PKB, p-Src, and p-Cav-1. The inhibitors for PI3K and Src significantly reversed the increase of p-Cav-1 induced by miR-132-3p. Moreover, overexpression of PTEN greatly reduced the endocytosis of cholera toxin subunit B and the up-regulation of p-Cav-1 induced by agomiR132-3p, suggesting that miR132-3p increases the endothelial permeability by inhibition of PTEN expression. In addition, miR132-3p significantly increased the delivery of doxorubicin across the BTB in vitro and contributed to the accumulation of doxorubicin within the brain tumor tissue. Our results show that miR-132-3p contributes to the increased permeability of BTB by targeting PTEN/PI3K/PKB/Src/Cav-1, thereby revealing a novel drug target for the treatment of brain gliomas.-Gu, Y., Cai, R., Zhang, C., Xue, Y., Pan, Y., Wang, J., Zhang, Z. miR-132-3p boosts caveolae-mediated transcellular transport in glioma endothelial cells by targeting PTEN/PI3K/PKB/Src/Cav-1 signaling pathway.

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Effects of mir-21 on Cardiac Microvascular Endothelial Cells After Acute Myocardial Infarction in Rats: Role of Phosphatase and Tensin Homolog (PTEN)/Vascular Endothelial Growth Factor (VEGF) Signal Pathway

Cited by 50 publications

References 42 publications

MicroRNA-145 is involved in endothelial cell dysfunction and acts as a promising biomarker of acute coronary syndrome

MicroRNA-145 is involved in endothelial cell dysfunction and acts as a promising biomarker of acute coronary syndrome

MicroRNA‐128 confers protection against cardiac microvascular endothelial cell injury in coronary heart disease via negative regulation of IRS1

miR‐132‐3p boosts caveolae‐mediated transcellular transport in glioma endothelial cells by targeting PTEN/PI3K/PKB/Src/Cav‐1 signaling pathway

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