期刊
HEART AND VESSELS
卷 36, 期 10, 页码 1597-1606出版社
SPRINGER
DOI: 10.1007/s00380-021-01853-8
关键词
Angiotensin II; MicroRNA-30d (miR-30d); Brain natriuretic peptide (BNP); Biomarker; Hypertension; Circulation miR
资金
- JSPS KAKEN [25460292]
- Japan Society for the Promotion of Science, Tokyo
The study was conducted to test the hypothesis that Ang II-induced cardiovascular complications can be distinguished from catecholamine-induced ones in rats based on their serum circulating biomarkers. It was found that serum microRNA-30d is a sensitive biomarker for Ang II-induced complications, while it is postulated that Ang II-induced cardiomyocyte hypertrophy may be independent of miR-30d/BNP signaling pathways.
We tested the hypothesis that angiotensin II (Ang II)-induced cardiovascular complications are distinguished from what catecholamine-induced by their serum circulating biomarkers in rats. Infusion of Ang II (1.68 mg/kg/day) significantly increased systolic and diastolic blood pressure assessed at week one or later, accompanied by an increase of heart/body weight ratio. Noradrenaline infusion (5.40 mg/kg/day) produced a similar degree of hypertension, but did not increase heart weight. Ang II-, but not noradrenaline-induced hypertension was associated with a drastic upregulation of serum microRNA-30d (miR-30d) by hundreds of times, accompanied by an increase of miR-30d levels in the atrium but not in the ventricle. Ang II, but not noradrenaline, significantly increased mRNA of brain natriuretic peptide (BNP) in the atrium. Studies using rat neonatal cardiomyocytes in vitro demonstrated that BNP caused an increase of miR-30d when applied for 6 h or longer in the culture medium. In vitro application of Ang II increased the cell size, although BNP and miR-30d were unable to mimic the effect of Ang II. We conclude that serum circulating microRNA-30d is a sensitive biomarker for Ang II-induced cardiovascular complications. It is also postulated that Ang II-induced cardiomyocyte hypertrophy could be independent of miR-30d/BNP signaling pathways.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据