Regulating effect of microRNA-21 on the expression of extracellular matrix of vascular smooth muscle cells under vascular remodeling of hypertension
10.3871/j.1004-7220.2015.01.001
- VernacularTitle:在高血压动脉重建中microRNA-21对血管平滑肌 细胞细胞外基质表达的调控作用
- Author:
Bao-rong SHEN
1
;
Qing-ping YAO
1
;
Guang-liang WU
1
;
Ying-xin QI
1
;
Zong-lai JIANG
1
Author Information
1. Institute of Mechanobiology & Medical Engineering, Shanghai Jiao Tong University
- Publication Type:Journal Article
- Keywords:
Cyclic strain;
Vascular smooth muscle cells (VSMCs);
Extracellular matrix (ECM);
Vascular remodeling;
Hypertension
- From:
Journal of Medical Biomechanics
2015;30(1):E001-E007
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the regulating effect and mechanism of microRNA-21 (miR-21) on extracellular matrix (ECM) of vascular smooth muscle cells (VSMCs) by vascular remodeling of hypertension. Methods By narrowing the abdominal aorta in rats, the hypertension models were established and divided into 2-week hypertension group and 4-week hypertension group, and sham-operated group was also established as control. VSMCs from the rat aorta were subjected to 0% (static), 5% (normal) and 15%（hypertensive）elongation strain at a constant frequency of 1.25 Hz and duration of 12 hours, respectively. The expressions of Smad 7 and ECM were detected by Western blotting, and the expression of miR-21 was examined by Real-time RT-PCR. Finally, miR-21 siRNA was used to study the role of miR-21 in the mechanical strain-induced expression of ECM, miR-21 and Smad 7. Results Compared with the sham-operated group, ECM and miR-21 in thoracic aorta of 2-week hypertension group were significantly elevated. Collagen I, collagen III and miR-21 in thoracic aorta of 4-week hypertension group were significantly elevated. Compared with the static and 5% strain groups, the protein expression of collagen I in VSMCs did not show significant change, but the protein expression of collagen III was significantly elevated and Smad 7 expression was significantly decreased in 15% strain group. The cyclic strain also enhanced miR-21 expression in VSMCs. miR-21 inhibitor effectively decreased the expression of miR-21 in VSMCs and protein level of collagen III, while enhanced Smad 7 expression under the static and 15% strain. Conclusions The vascular remodeling of hypertension causes the high expressions of ECM and miR-21. The cyclic strain induces the high expression of miR-21, which via Smad 7 results in enhancing the expression of ECM, collagen III especially, in VSMCs under vascular remodeling of hypertension.
