MicroRNA-155 inhibits angiotensin II-induced vascular smooth muscle cell proliferation

Yang, Lixia; Gao, Liu; Zhu, Guofu; Liu, Hong; Guo, R. S.; Qi, Feng; Zou, Jihong

doi:10.1177/1470320313503693

Cited by 36 publications

(19 citation statements)

References 26 publications

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“…MiRs‐ 150, 155, and 181b are anti‐inflammatory via indirect regulation of NF‐kB (Cheng, Njock, Khyzha, Dang, & Fish, 2014; Luo et al., 2018). MiR‐155 may also have pro‐inflammatory effects, and acts to regulate smooth muscle cell function by directly targeting eNOS and angiotensin II type I receptor expression (Sun et al., 2012; Yang et al., 2014; Zhang, Zhao, Yu, Lu, & Zheng, 2015). The greater and/or specific increases in these ci‐miRs after HII could both reflect and perpetuate a greater anti‐inflammatory response to the HII exercise bout as compared to the MOD bout, although we found no significant correlations between changes in these ci‐miRs and measures of arterial stiffness.…”

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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“…In ECs, Ang II induced expression of ET-1, a target of miR-155 and a key regulator in vascular inflammation and remodeling (160, 161). Overexpression of miR-155 reduced: (i) Ang II-mediated migration and inflammatory activation of ECs (162), (ii) AT1R expression in Ang II-treated hypertrophic cardiomyocytes (161), and (iii) Ang II-induced VSMSc proliferation (163). …”

Section: Mirnas In Hypertensionmentioning

confidence: 99%

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Lucia

Komici²,

Borghetti

et al. 2017

Front. Med.

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Over the last decades, life expectancy has significantly increased although several chronic diseases persist in the population, with aging as the leading risk factor. Despite improvements in diagnosis and treatment, many elderlies suffer from cardiovascular problems that are much more frequent in an older, more fragile organism. In the long term, age-related cardiovascular diseases (CVDs) contribute to the decline of quality of life and ability to perform normal activities of daily living. microRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene expression at the posttranscriptional level in both physiological and pathological conditions. In this review, we will focus on the role of miRNAs in aging and age-related CVDs as heart failure, hypertension, atherosclerosis, atrial fibrillation, and diabetes mellitus. miRNAs are key regulators of complex biological mechanisms, representing an exciting potential therapeutic target in CVDs. Moreover, one major challenge in geriatric medicine is to find reliable biomarkers for diagnosis, prognosis, and prediction of the response to specific drugs. miRNAs represent a very promising tool due to their stability in the circulation and unique signature in CVDs. However, further studies are needed to investigate their translational potential in the real clinical practice.

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“…Specifically, overexpression of miR-223 and miR-153 inhibited stretch stress-enhanced VSMCs proliferation via activation of the insulin-like growth factor-1 receptor and PI3K-AKT signaling pathway [113]. Besides, miR-155 and miR-217 would inhibit angiotensin II and homocysteine-induced VSMC proliferation and migration [114, 115]. In contrast, miR-132 and miR-125b could block VSMC proliferation and neointimal hyperplasia in atherosclerosis [116, 117].…”

Section: Mirnas and Vascular Agingmentioning

confidence: 99%

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Lin

Zhan

Wang

et al. 2016

BioMed Research International

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Vascular aging, a specific type of organic aging, is related to age-dependent changes in the vasculature, including atherosclerotic plaques, arterial stiffness, fibrosis, and increased intimal thickening. Vascular aging could influence the threshold, process, and severity of various cardiovascular diseases, thus making it one of the most important risk factors in the high mortality of cardiovascular diseases. As endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell biological basis of these pathology changes of the vasculature, the structure and function of ECs and VSMCs play a key role in vascular aging. MicroRNAs (miRNAs), small noncoding RNAs, have been shown to regulate the expression of multiple messenger RNAs (mRNAs) posttranscriptionally, contributing to many crucial aspects of cell biology. Recently, miRNAs with functions associated with aging or aging-related diseases have been studied. In this review, we will summarize the reported role of miRNAs in the process of vascular aging with special emphasis on EC and VSMC functions. In addition, the potential application of miRNAs to clinical practice for the diagnosis and treatment of cardiovascular diseases will also be discussed.

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MicroRNA-155 inhibits angiotensin II-induced vascular smooth muscle cell proliferation

Abstract: miR-155 downregulation of Ang II-induced VSMC viability identifies it as an important regulator of cell proliferation.

Cited by 36 publications

References 26 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

microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

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