Localization of Adenylyl Cyclase Isoforms and G Protein-Coupled Receptors in Vascular Smooth Muscle Cells: Expression in Caveolin-Rich and Noncaveolin Domains

2002 ◽  
Vol 62 (5) ◽  
pp. 983-992 ◽  
Author(s):  
Rennolds S. Ostrom ◽  
Xiaoqiu Liu ◽  
Brian P. Head ◽  
Caroline Gregorian ◽  
Tammy M. Seasholtz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Adenylyl Cyclase ◽  
G Protein ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
G Protein Coupled Receptors ◽  
G Protein Coupled

scholarly journals Selective Activation of Nuclear Phospholipase D-1 by G Protein–Coupled Receptor Agonists in Vascular Smooth Muscle Cells

2006 ◽  
Vol 99 (2) ◽  
pp. 132-139 ◽  
Author(s):  
Stéphanie Gayral ◽  
Paul Déléris ◽  
Karine Laulagnier ◽  
Muriel Laffargue ◽  
Jean-Pierre Salles ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
G Protein ◽  
Vascular Smooth Muscle Cells ◽  
Phospholipase D ◽  
Muscle Cells ◽  
G Protein Coupled Receptor ◽  
Selective Activation ◽  
G Protein Coupled

scholarly journals G Protein-coupled Receptor Kinase 5 in Cultured Vascular Smooth Muscle Cells and Rat Aorta

1997 ◽  
Vol 272 (51) ◽  
pp. 32482-32488 ◽  
Author(s):  
Nobukazu Ishizaka ◽  
R. Wayne Alexander ◽  
Jørn Bech Laursen ◽  
Hisashi Kai ◽  
Toshiki Fukui ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
G Protein ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

scholarly journals RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (7) ◽  
pp. e0180842 ◽  
Author(s):  
Danielle Kamato ◽  
Venkata Vijayanand Bhaskarala ◽  
Nitin Mantri ◽  
Tae Gyu Oh ◽  
Dora Ling ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Rna Sequencing ◽  
G Protein ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Receptor Signalling ◽  
G Protein Coupled ◽  
Receptor Transactivation

scholarly journals Role of integrins in angiotensin II-induced proliferation of vascular smooth muscle cells

2011 ◽  
Vol 300 (3) ◽  
pp. C647-C656 ◽  
Author(s):  
Marlene A. Bunni ◽  
Inga I. Kramarenko ◽  
Linda Walker ◽  
John R. Raymond ◽  
Maria N. Garnovskaya
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
G Protein ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Erk Activation ◽  
G Protein Coupled

Angiotensin II (AII) binds to G protein-coupled receptor AT1 and stimulates extracellular signal-regulated kinase (ERK), leading to vascular smooth muscle cells (VSMC) proliferation. Proliferation of mammalian cells is tightly regulated by adhesion to the extracellular matrix, which occurs via integrins. To study cross-talk between G protein-coupled receptor- and integrin-induced signaling, we hypothesized that integrins are involved in AII-induced proliferation of VSMC. Using Oligo GEArray and quantitative RT-PCR, we established that messages for α1-, α5-, αV-, and β1-integrins are predominant in VSMC. VSMC were cultured on plastic dishes or on plates coated with either extracellular matrix or poly-d-lysine (which promotes electrostatic cell attachment independent of integrins). AII significantly induced proliferation in VSMC grown on collagen I or fibronectin, and this effect was blocked by the ERK inhibitor PD-98059, suggesting that AII-induced proliferation requires ERK activity. VSMC grown on collagen I or on fibronectin demonstrated approximately three- and approximately sixfold increases in ERK phosphorylation after stimulation with 100 nM AII, respectively, whereas VSMC grown on poly-d-lysine demonstrated no significant ERK activation, supporting the importance of integrin-mediated adhesion. AII-induced ERK activation was reduced by >65% by synthetic peptides containing an RGD (arginine-glycine-aspartic acid) sequence that inhibit α5β1-integrin, and by ∼60% by the KTS (lysine-threonine-serine)-containing peptides specific for integrin-α1β1. Furthermore, neutralizing antibody against β1-integrin and silencing of α1, α5, and β1 expression by transfecting VSMC with short interfering RNAs resulted in decreased AII-induced ERK activation. This work demonstrates roles for specific integrins (most likely α5β1 and α1β1) in AII-induced proliferation of VSMC.

IV. Neural regulation of gastrointestinal smooth muscle

1998 ◽  
Vol 275 (1) ◽  
pp. G1-G7 ◽  
Author(s):  
Kenton M. Sanders
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Adenylyl Cyclase ◽  
G Protein ◽  
Interstitial Cells Of Cajal ◽  
Muscle Cells ◽  
G Protein Coupled Receptors ◽  
Muscle Tissues ◽  
Cells Of Cajal ◽  
G Protein Coupled

G protein-coupled receptors receive many of the neural, hormonal, and paracrine inputs to gastrointestinal (GI) smooth muscle cells. This article examines the major G protein-coupled receptors, G proteins, and effectors that mediate responses to enteric neuromuscular transmitters. Excitatory transmitters primarily couple through Gq/11 and Gi/Goproteins and elicit responses via formation of inositol trisphosphate and diacylglycerol and inhibition of adenylyl cyclase. Several inhibitory transmitters couple through Gs and activation of adenylyl cyclase. There are interesting examples, however, of inhibitory transmitters apparently using pathways regulated by Gq/11 to elicit responses by localized Ca2+ release and activation of Ca2+-dependent ion channels. G protein-coupled receptors may also be differentially expressed by smooth muscle cells and interstitial cells of Cajal, which may increase the diversity of responses and allow specialized innervation of GI muscle tissues.

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