scholarly journals Intrinsic circadian oscillation of myosin light chain phosphorylation in vascular smooth muscle cells

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Toshiro Saito ◽  
Mayumi Hirano ◽  
Tomomi Ide ◽  
Kenji Sunagawa ◽  
Katsuya Hirano
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Muscle Cells ◽  
Circadian Oscillation ◽  
Myosin Light Chain Phosphorylation

scholarly journals Apelin Stimulates Myosin Light Chain Phosphorylation in Vascular Smooth Muscle Cells

2006 ◽  
Vol 26 (6) ◽  
pp. 1267-1272 ◽  
Author(s):  
Tatsuo Hashimoto ◽  
Minoru Kihara ◽  
Junji Ishida ◽  
Nozomi Imai ◽  
Shin-ichiro Yoshida ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Muscle Cells ◽  
Myosin Light Chain Phosphorylation

scholarly journals Rapid effects of aldosterone on clonal human vascular smooth muscle cells

2007 ◽  
Vol 292 (2) ◽  
pp. C788-C794 ◽  
Author(s):  
Robert Gros ◽  
Qingming Ding ◽  
Souzan Armstrong ◽  
Caroline O'Neil ◽  
J. Geoffrey Pickering ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Muscle Cells ◽  
Myosin Light Chain Phosphorylation ◽  
Phosphatidylinositol 3 Kinase ◽  
Dose Dependent

It has been increasingly appreciated that aldosterone elicits acute vascular effects through nongenomic signaling pathways. Our previous studies demonstrated that aldosterone attenuated phenylephrine-mediated constriction in intact vessels [via phosphatidylinositol 3-kinase-dependent nitric oxide synthase activation] but enhanced vasoconstrictor responses in endothelium-denuded arteries. To determine the mechanism of this vasoconstrictor response, we assessed the effect of aldosterone on myosin light-chain phosphorylation and contraction in clonal adult human vascular smooth muscle cells. Acute aldosterone exposure mediated dose-dependent myosin light-chain phosphorylation, inhibited by spironolactone and phosphatidylinositol 3-kinase inhibition. These rapid effects of aldosterone were mimicked by estradiol and hydrocortisone and were also inhibitable by both spironolactone and eplerenone. In parallel to its effects on myosin light-chain phosphorylation, aldosterone mediated dose-dependent contraction responses that were inhibited by spironolactone. Comparable contractile responses were seen with both 17β-estradiol and hydrocortisone. In total, these data are consistent with a mechanism of acute aldosterone-mediated contraction common to both glucocorticoids and estrogen. Steroid-mediated vasoconstriction may represent an important pathobiological mechanism of vascular disease, especially in the setting of preexisting endothelial dysfunction.

scholarly journals 2-Methoxyestradiol blocks the RhoA/ROCK1 pathway in human aortic smooth muscle cells

2015 ◽  
Vol 309 (12) ◽  
pp. E995-E1007 ◽  
Author(s):  
Lisa Rigassi ◽  
Federica Barchiesi Bozzolo ◽  
Eliana Lucchinetti ◽  
Michael Zaugg ◽  
Jürgen Fingerle ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Molecular Mechanisms ◽  
Muscle Cells ◽  
Myosin Phosphatase ◽  
Downstream Signaling

2-Methoxyestradiol (2-ME), a metabolite of estradiol with little affinity for estrogen receptors, inhibits proliferation of vascular smooth muscle cells; however, the molecular mechanisms underlying this effect are incompletely understood. Our previous work shows that 2-ME inhibits initiation (blocks phosphorylation of ERK and Akt) and progression (reduces cyclin expression and increases expression of cyclin inhibitors) of the mitogenic pathway and interferes with mitosis (disrupts tubulin organization). Because the RhoA/ROCK1 pathway (RhoA → ROCK1 → myosin phosphatase targeting subunit → myosin light chain) is involved in cytokinesis, herein we tested the concept that 2-ME also blocks the RhoA/ROCK1 pathway. Because of the potential importance of 2-ME for preventing/treating vascular diseases, experiments were conducted in female human aortic vascular smooth muscle cells. Microarray transcriptional profiling suggested an effect of 2-ME on the RhoA/ROCK1 pathway. Indeed, 2-ME blocked mitogen-induced GTP-bound RhoABC expression and membrane-bound RhoA, suggesting interference with the activation of RhoA. 2-ME also reduced ROCK1 expression, suggesting reduced production of the primary downstream signaling kinase of the RhoA pathway. Moreover, 2-ME inhibited RhoA/ROCK1 pathway downstream signaling, including phosphorylated myosin phosphatase targeting subunit and myosin light chain; the ROCK1 inhibitor H-1152 mimicked these effects of 2-ME; both 2-ME and H-1152 blocked cytokinesis. 2-ME also reduced the expression of tissue factor, yet another downstream signaling component of the RhoA/ROCK1 pathway. We conclude that 2-ME inhibits the pathway RhoA → ROCK1 → myosin phosphatase targeting subunit → myosin light chain, and this likely contributes to the reduced cytokinesis in 2-ME treated HASMCs.

Sign in / Sign up

Export Citation Format

Share Document