scholarly journals MiR-204 regulates type 1 IP3R to control vascular smooth muscle cell contractility and blood pressure

Cell Calcium ◽  
2019 ◽  
Vol 80 ◽  
pp. 18-24 ◽  
Author(s):  
Mohanad Gabani ◽  
Jing Liu ◽  
Karima Ait-Aissa ◽  
Olha Koval ◽  
Young-Rae Kim ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Contractility

scholarly journals Vascular smooth muscle cell contractile protein expression is increased through protein kinase G-dependent and -independent pathways by glucose-6-phosphate dehydrogenase inhibition and deficiency

2016 ◽  
Vol 311 (4) ◽  
pp. H904-H912 ◽  
Author(s):  
Sukrutha Chettimada ◽  
Sachindra Raj Joshi ◽  
Vidhi Dhagia ◽  
Alessandro Aiezza ◽  
Thomas M. Lincoln ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Contractile Proteins ◽  
Protein Kinase G ◽  
Glucose 6 Phosphate Dehydrogenase

Homeostatic control of vascular smooth muscle cell (VSMC) differentiation is critical for contractile activity and regulation of blood flow. Recently, we reported that precontracted blood vessels are relaxed and the phenotype of VSMC is regulated from a synthetic to contractile state by glucose-6-phosphate dehydrogenase (G6PD) inhibition. In the current study, we investigated whether the increase in the expression of VSMC contractile proteins by inhibition and knockdown of G6PD is mediated through a protein kinase G (PKG)-dependent pathway and whether it regulates blood pressure. We found that the expression of VSMC-restricted contractile proteins, myocardin (MYOCD), and miR-1 and miR-143 are increased by G6PD inhibition or knockdown. Importantly, RNA-sequence analysis of aortic tissue from G6PD-deficient mice revealed uniform increases in VSMC-restricted genes, particularly those regulated by the MYOCD-serum response factor (SRF) switch. Conversely, expression of Krüppel-like factor 4 (KLF4) is decreased by G6PD inhibition. Interestingly, the G6PD inhibition-induced expression of miR-1 and contractile proteins was blocked by Rp-β-phenyl-1, N2-etheno-8-bromo-guanosine-3′,5′-cyclic monophosphorothioate, a PKG inhibitor. On the other hand, MYOCD and miR-143 levels are increased by G6PD inhibition through a PKG-independent manner. Furthermore, blood pressure was lower in the G6PD-deficient compared with wild-type mice. Therefore, our results suggest that the expression of VSMC contractile proteins induced by G6PD inhibition occurs via PKG1α-dependent and -independent pathways.

scholarly journals Angiotensin II Induces Vascular Smooth Muscle Cell Replication Independent of Blood Pressure

Hypertension ◽  
1998 ◽  
Vol 31 (6) ◽  
pp. 1331-1337 ◽  
Author(s):  
Enming J. Su ◽  
Donna M. Lombardi ◽  
Justin Siegal ◽  
Stephen M. Schwartz
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Replication
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