MicroRNA-126 enhances the biological function of endothelial progenitor cells under oxidative stress via PI3K/Akt/GSK-3β and ERK1/2 signaling pathways

Qing, WU; B, Qi; Duan, Xiaoyu; Xin, Ming; Yan, Fengqin; He, Yuhong; Bu, Xiaofen; Sun, Shan; Hong, Zhu

doi:10.17305/bjbms.2019.4493

Cited by 15 publications

(9 citation statements)

References 44 publications

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“…Overexpression of miR-126 could revert the injury in EPCs by reducing oxidative stress as demonstrated by decreased ROS and MDA production and increased SOD, angiopoietin (Ang) 1, and Ang2 expression. Although the authors did not investigate the specific gene targeting through which miR-126 exerts its antioxidant function, they showed a direct activation of PI3K/Akt/SK-3b and ERK1/2 signaling pathway by miR-126, which contributed to the biological functions of EPCs [70]. Sirt1, which is known to deacetylate Akt and promote its activation, might be involved in the miR-126 regulation of this pathway.…”

Section: Crosstalk Between Mirnas and The Sirtuin Family In MImentioning

confidence: 99%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

101

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Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

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Section: Crosstalk Between Mirnas and The Sirtuin Family In MImentioning

confidence: 99%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

101

View full text Add to dashboard Cite

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“…Akt activation is a critical step to phosphorylate GSK3β in glycogen synthesis process. It is evidenced that miR-126 enhances the biological function of EPCs under oxidative stress via PI3K/Akt/GSK3β signaling pathways [ 98 ]. Interestingly, there is an increase in cardiac IRS1-PI3K activity and a reduction of GLUT4 in patients with T2DM [ 38 ].…”

Section: Mechanism Of Exercise-induced Mir-126 In Improving Cardiovas...mentioning

confidence: 99%

Roles of physical exercise-induced MiR-126 in cardiovascular health of type 2 diabetes

Liu

Wang

et al. 2022

Diabetol Metab Syndr

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Although physical activity is widely recommended for preventing and treating cardiovascular complications of type 2 diabetes mellitus (T2DM), the underlying mechanisms remain unknown. MicroRNA-126 (miR-126) is an angiogenetic regulator abundant in endothelial cells (ECs) and endothelial progenitor cells (EPCs). It is primarily involved in angiogenesis, inflammation and apoptosis for cardiovascular protection. According to recent studies, the levels of miR-126 in the myocardium and circulation are affected by exercise protocol. High-intensity interval training (HIIT) or moderate-and high-intensity aerobic exercise, whether acute or chronic, can increase circulating miR-126 in healthy adults. Chronic aerobic exercise can effectively rescue the reduction of myocardial and circulating miR-126 and vascular endothelial growth factor (VEGF) in diabetic mice against diabetic vascular injury. Resistance exercise can raise circulating VEGF levels, but it may have a little influence on circulating miR-126. The Several targets of miR-126 have been suggested for cardiovascular fitness, such as sprouty-related EVH1 domain-containing protein 1 (SPRED1), phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2), vascular cell adhesion molecule 1 (VCAM1), high-mobility group box 1 (HMGB1), and tumor necrosis factor receptor-associated factor 7 (TRAF7). Here, we present a comprehensive review of the roles of miR-126 and its downstream proteins as exercise mechanisms, and propose that miR-126 can be applied as an exercise indicator for cardiovascular prescriptions and as a preventive or therapeutic target for cardiovascular complications in T2DM.

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“…Otherwise, recent data represent that miR-126 overexpression significantly increases the protein expression of the PI3K, Akt, GSK3β, and ERK1/2 signaling pathways and attenuates ROS vascular content [ 111 ]. Another research project reported that miR-126 negatively regulates vascular endothelial growth factor expression in hypoxia-induced monkey chorioretinal vessel endothelial cells [ 112 ].…”

Section: Discussionmentioning

confidence: 99%

Partial Synthetic PPARƳ Derivative Ameliorates Aorta Injury in Experimental Diabetic Rats Mediated by Activation of miR-126-5p Pi3k/AKT/PDK 1/mTOR Expression

et al. 2022

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Type 2 diabetes mellitus (T2D) is a world wild health care issue marked by insulin resistance, a risk factor for the metabolic disorder that exaggerates endothelial dysfunction, increasing the risk of cardiovascular complications. Peroxisome proliferator-activated receptor PPAR) agonists have therapeutically mitigated hyperlipidemia and hyperglycemia in T2D patients. Therefore, we aimed to experimentally investigate the efficacy of newly designed synthetic PPARα/Ƴ partial agonists on a High-Fat Diet (HFD)/streptozotocin (STZ)-induced T2D. Female Wistar rats (200 ± 25 g body weight) were divided into four groups. The experimental groups were fed the HFD for three consecutive weeks before STZ injection (45 mg/kg/i.p) to induce T2D. Standard reference PPARƳ agonist pioglitazone and the partial synthetic PPARƳ (PIO; 20 mg/kg/BW, orally) were administered orally for 2 weeks after 72 h of STZ injection. The aorta tissue was isolated for biological ELISA, qRT-PCR, and Western blotting investigations for vascular inflammatory endothelial mediators endothelin-1 (ET-1), intracellular adhesion molecule 1 (ICAM-1), E-selectin, and anti-inflammatory vasoactive intestinal polypeptide (VIP), as well as microRNA126-5p and p-AKT/p-Pi3k/p-PDK-1/p-mTOR, endothelial Nitric Oxide Synthase (eNOS) immunohistochemical staining all are coupled with and histopathological examination. Our results revealed that HFD/STZ-induced T2D increased fasting blood glucose, ET-1, ICAM-1, E-selectin, and VIP levels, while decreasing the expression of both microRNA126-5p and p-AKT/p-Pi3k/p-PDK-1/p-mTOR phosphorylation. In contrast, the partial synthetic PPARƳ derivative evidenced a vascular alteration significantly more than reference PIO via decreasing (ET-1), ICAM-1, E-selectin, and VIP, along with increased expression of microRNA126-5p and p-AKT/p-Pi3k/p-PDK-1/p-mTOR. In conclusion, the partial synthetic PPARƳ derivative significantly affected HFD/STZ-induced T2D with vascular complications in the rat aorta.

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MicroRNA-126 enhances the biological function of endothelial progenitor cells under oxidative stress via PI3K/Akt/GSK-3β and ERK1/2 signaling pathways

Cited by 15 publications

References 44 publications

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Roles of physical exercise-induced MiR-126 in cardiovascular health of type 2 diabetes

Partial Synthetic PPARƳ Derivative Ameliorates Aorta Injury in Experimental Diabetic Rats Mediated by Activation of miR-126-5p Pi3k/AKT/PDK 1/mTOR Expression

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