|  Help  |  About  |  Contact Us

Publication : HuR (Human Antigen R) Regulates the Contraction of Vascular Smooth Muscle and Maintains Blood Pressure.

First Author  Liu S Year  2020
Journal  Arterioscler Thromb Vasc Biol Volume  40
Issue  4 Pages  943-957
PubMed ID  32075416 Mgi Jnum  J:307307
Mgi Id  MGI:6709712 Doi  10.1161/ATVBAHA.119.313897
Citation  Liu S, et al. (2020) HuR (Human Antigen R) Regulates the Contraction of Vascular Smooth Muscle and Maintains Blood Pressure. Arterioscler Thromb Vasc Biol 40(4):943-957
abstractText  OBJECTIVE: HuR (human antigen R)-an RNA-binding protein-is involved in regulating mRNA stability by binding adenylate-uridylate-rich elements. This study explores the role of HuR in the regulation of smooth muscle contraction and blood pressure. Approach and Results: Vascular HuR(SMKO) (smooth muscle-specific HuR knockout) mice were generated by crossbreeding HuR(flox/flox) mice with alpha-SMA (alpha-smooth muscle actin)-Cre mice. As compared with CTR (control) mice, HuR(SMKO) mice showed hypertension and cardiac hypertrophy. HuR levels were decreased in aortas from hypertensive patients and SHRs (spontaneously hypertensive rats), and overexpression of HuR could lower the blood pressure of SHRs. Contractile response to vasoconstrictors was increased in mesenteric artery segments isolated from HuR(SMKO) mice. The functional abnormalities in HuR(SMKO) mice were attributed to decreased mRNA and protein levels of RGS (regulator of G-protein signaling) protein(s) RGS2, RGS4, and RGS5, which resulted in increased intracellular calcium increase. Consistently, the degree of intracellular calcium ion increase in HuR-deficient smooth muscle cells was reduced by overexpression of RGS2, RGS4, or RGS5. Finally, administration of RGS2 and RGS5 reversed the elevated blood pressure in HuR(SMKO) mice. CONCLUSIONS: Our findings indicate that HuR regulates vascular smooth muscle contraction and maintains blood pressure by modulating RGS expression.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Bio Entities

Trail: Publication

0 Expression