MicroRNA-221 regulates endothelial nitric oxide production and inflammatory response by targeting adiponectin receptor 1

Chen, Chaofeng; Huang, Jinyu; Li, Hong; Chu, Zun-hua; Huang, Xin; Tong, Guoxiang; Xu, Yizhou

doi:10.1016/j.gene.2015.04.014

Cited by 43 publications

(35 citation statements)

References 30 publications

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“…Within endothelial and smooth muscle cells, miR‐221 is anti‐angiogenic and anti‐inflammatory (Celic, Metzinger‐Le Meuth, Six, Massey, & Metzinger, 2016; Chistiakov, Sobenin, Orekhov, & Bobryshev, 2015). It can also increase ROS production by directly targeting PGC‐1α and adiponectin receptor I (Chen et al., 2015; Xue et al., 2015). Changes in ci‐miR‐221‐3p correlated positively with the change in cf‐PWV 60 min after exercise, while only changes in ci‐miR‐21‐5p were positively associated with the change in cf‐PWV 10 min after exercise.…”

Section: Discussionmentioning

confidence: 99%

Changes in circulating microRNA and arterial stiffness following high‐intensity interval and moderate intensity continuous exercise

et al. 2020

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High-intensity interval (HII) exercise elicits distinct vascular responses compared to a matched dose of moderate intensity continuous (MOD) exercise. However, the acute effects of HII compared to MOD exercise on arterial stiffness are incompletely understood. Circulating microRNAs (ci-miRs) may contribute to the vascular effects of exercise. We sought to determine exercise intensity-dependent changes in ci-miR potentially underlying changes in arterial stiffness. Ten young, healthy men underwent well-matched, 30-min HII and MOD exercise bouts. RT-qPCR was used to determine the levels of seven vascular-related ci-miRs in serum obtained immediately before and after exercise. Arterial stiffness measures including carotid to femoral pulse wave velocity (cf-PWV), carotid arterial compliance and β-stiffness, and augmentation index (AIx and AIx75) were taken before, 10min after and 60min after exercise. Ci-miR-21-5p, 126-3p, 126-5p, 150-5p, 155-5p, and 181b-5p increased after HII exercise (p < .05), while ci-miR-150-5p and 221-3p increased after MOD exercise (p = .03 and 0.056). One hour after HII exercise, cf-PWV trended toward being lower compared to baseline (p = .056) and was significantly lower compared to 60min after MOD exercise (p = .04). Carotid arterial compliance was increased 60min after HII exercise (p = .049) and was greater than 60min after MOD exercise (p = .02). AIx75 increased 10 min after both HII and MOD exercise (p < .05).There were significant correlations between some of the exercise-induced changes in individual ci-miRs and changes in cf-PWV and AIx/AIx75. These results support the hypotheses that arterial stiffness and ci-miRs are altered in an exercise intensitydependent manner, and ci-miRs may contribute to changes in arterial stiffness.

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Section: Discussionmentioning

confidence: 99%

Changes in circulating microRNA and arterial stiffness following high‐intensity interval and moderate intensity continuous exercise

et al. 2020

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“…As post-transcriptional regulators of gene expression, microRNAs may be partly responsible for the disparate expression of adiponectin receptors at the protein and RNA levels. A recent bioinformatics analysis showed that adiponectin signaling is regulated by microRNAs: miR-221 inhibits AdipoR1 expression, which suggests that miR-221 regulates AdipoR1 signaling in different pathological processes (Chen et al, 2015). On the other hand, AdipoR2 has been identified as a direct target of miR-218 (Du et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Adiponectin Receptors Are Less Sensitive to Stress in a Transgenic Mouse Model of Alzheimer's Disease

et al. 2017

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Background: Adiponectin and leptin are implicated in the initiation and pathomechanism of Alzheimer's disease (AD). The serum concentrations of these adipokines has been extensively studied in AD, however little is known about their receptors in this disease.Objective: We developed a novel approach to examine whether the receptors of adiponectin (AdipoR1 and -R2) and/or leptin (LepR) can contribute to AD pathomechanism. To achieve this, we investigated the effect of both genetic and environmental factors associated with AD on the expression of these receptors.Method: We used C57BL/6J (WT) and APP(swe)/Presen(e9d)1 (AD) mice. Both strains were exposed to restraint stress (RS) daily for 6h over different time periods. Then, we measured the mRNA expression of AdipoR1, AdipoR2 and LepR and the level of AdipoR1 and AdipoR2 proteins in the hippocampal and prefrontal cortical areas of each mouse.Results: We detected brain region specific transcriptomic changes of adiponectin receptors induced by APP and PS1 transgenes. Both acute and chronic RS caused significant elevations in AdipoR1 mRNA expression in the hippocampus of WT mice. In the prefrontal cortex, the mRNA expression of AdipoR1 followed a biphasic course. In AD mice, RS did not promote any changes in the expression of AdipoR1 mRNA and AdipoR1 protein levels. AdipoR2 mRNA in AD animals, however, showed a significant increase in the prefrontal cortex during RS. Regarding AdipoR1 and AdipoR2 mRNA and protein expression, relevant changes could be measured during stress exposure in both brain areas. Furthermore, stress exposed groups exhibited little change in LepR mRNA expression.Conclusion: Our findings indicate that carrying the transgenes associated with AD induces modification in the expression of both adiponectin receptors. In the case of a normal genetic background, these receptors also appear to be sensitive to environmental factors, while in a genetically determined AD model less response to stress stimuli could be observed. The results suggest that modification of adipokine receptors could also be considered in the therapeutic approach to AD.

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“…9 Reducing the oxidative stress by antioxidant or thiol reductant treatment, or overexpression of thioredoxin or manganese superoxide could largely ameliorate apoptosis. [12][13][14] Accumulating evidence demonstrates that miR-221 is functionally imperative in the regulation of cell apoptosis, 15 inflammatory response, 16 coronary heart diseases, 17 and cancers. [12][13][14] Accumulating evidence demonstrates that miR-221 is functionally imperative in the regulation of cell apoptosis, 15 inflammatory response, 16 coronary heart diseases, 17 and cancers.…”

Section: Introductionmentioning

confidence: 99%

miR‐221‐3p inhibits oxidized low‐density lipoprotein induced oxidative stress and apoptosis via targeting a disintegrin and metalloprotease‐22

Zhuang

Maimaitijiang

et al. 2018

J of Cellular Biochemistry

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Oxidized low‐density lipoprotein (ox‐LDL)‐induced oxidative stress and apoptosis are considered as a critical contributor to atherosclerosis. MicroRNAs (miRNAs) have been reported versatile functions in all biological processes via directly suppressing target messenger RNA at a posttranscriptional level. Although miRNA‐221 has been implied to be involved in the regulation of atherosclerosis, the underlying mechanism remains unclear. Here, we showed that ox‐LDL treatment remarkably suppressed the expression of miR‐221‐3p in a concentration‐dependent and time‐dependent manner. Transfection of miR‐221‐3p mimic significantly reduced the foam cell formation and expression of lipid biomarkers, while transfection of the miR‐221‐3p inhibitor showed completely opposite effects. Moreover, miR‐221‐3p was also found to inhibit the process of cell apoptosis in macrophages. A disintegrin and metalloprotease‐22 (ADAM22) is predicted as a direct target of miR‐221‐3p, and silencing AMAM22 resulted in a reduced foam cell formation and cell apoptosis. Furthermore, silencing AMAM22 restored the stimulatory effect of the miR‐221‐3p inhibitor in ox‐LDL‐induced foam cell formation and apoptosis. These findings suggest that miR‐221‐3p inhibits ox‐LDL and apoptosis via directly targeting ADAM22.

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MicroRNA-221 regulates endothelial nitric oxide production and inflammatory response by targeting adiponectin receptor 1

Cited by 43 publications

References 30 publications

Changes in circulating microRNA and arterial stiffness following high‐intensity interval and moderate intensity continuous exercise

Changes in circulating microRNA and arterial stiffness following high‐intensity interval and moderate intensity continuous exercise

Adiponectin Receptors Are Less Sensitive to Stress in a Transgenic Mouse Model of Alzheimer's Disease

miR‐221‐3p inhibits oxidized low‐density lipoprotein induced oxidative stress and apoptosis via targeting a disintegrin and metalloprotease‐22

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