Excitatory Agonists and Ca-Permeable Channels in Arterial Smooth Muscle Cells

1989 ◽  
pp. 45-56 ◽  
Author(s):  
Ingrid Declerck ◽  
Guy Droogmans ◽  
Rik Casteels
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells

scholarly journals Effects of vasopressin on ATP-sensitive and Ca2+-activated K+ channels of coronary arterial smooth muscle cells

1992 ◽  
Vol 58 ◽  
pp. 339
Author(s):  
Tetsuzo Wakatsuki ◽  
Yutaka Nakaya ◽  
Yukiko Miyoshi ◽  
Zeng Xiao-Rong ◽  
Masahiro Nomura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Arterial Smooth Muscle Cells

Propagation of fast and slow intercellular Ca2+ waves in primary cultured arterial smooth muscle cells

Cell Calcium ◽  
2011 ◽  
Vol 50 (5) ◽  
pp. 459-467 ◽  
Author(s):  
Nadia Halidi ◽  
François-Xavier Boittin ◽  
Jean-Louis Bény ◽  
Jean-Jacques Meister
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells

scholarly journals Epoxyeicosatrienoic acid metabolism in arterial smooth muscle cells.

1995 ◽  
Vol 36 (6) ◽  
pp. 1236-1246 ◽  
Author(s):  
X. Fang ◽  
M. VanRollins ◽  
T.L. Kaduce ◽  
A.A. Spector
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Acid Metabolism ◽  
Muscle Cells ◽  
Epoxyeicosatrienoic Acid ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells

Independence of growth factor induced plasminogen activator inhibitor type-1 (PAI-1) expression from the 4G/5G polymorphism of the PAI-1 gene

2003 ◽  
Vol 90 (07) ◽  
pp. 36-42 ◽  
Author(s):  
Esther Eschenfelder ◽  
Karlheinz Peter ◽  
Burton Sobel ◽  
Christoph Bode ◽  
Thomas Nordt
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Smooth Muscle Cells ◽  
Genetic Factors ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Gene And Protein Expression ◽  
Arterial Smooth Muscle Cells ◽  
Pai 1

SummaryIncreased PAI-1 expression has been implicated in accelerating atherogenesis. Increases under some conditions are modulated by growth factors. Genetic factors such as the 4G/5G poly-morphism in the promoter of the PAI-1 gene play a role under certain circumstances. The present study was designed to delineate for the first time interactions between growth factors and the 4G/5G polymorphism with respect to PAI-1 expression in human arterial smooth muscle cells (HASMC).HASMC were genotyped and exposed to growth factors. PAI-1 gene and protein expression were induced consistently by TGF-β (up to 4.0-fold), PDGF (2.1-fold),TNF-α (1.7-fold), and thrombin (2.3-fold). Results were similar regardless of which genotype (4G/4G [n=9], 4G/5G [n=13], and 5G/5G [n=7]) was present.The induction of increased PAI-1 expression in human arterial smooth muscle cells by growth factors implicated in accelerated atherogenesis is independent of the PAI-1 4G/5G polymorphism. Accordingly, modulation of PAI-1 expression is likely to be influenced predominantly by environmental factors acting on, rather than genetic factors intrinsic to the PAI-1 promoter.

Exogenous ATP induces a limited cell cycle progression of arterial smooth muscle cells

1993 ◽  
Vol 264 (4) ◽  
pp. C783-C788 ◽  
Author(s):  
R. Malam-Souley ◽  
M. Campan ◽  
A. P. Gadeau ◽  
C. Desgranges
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cell Cycle Progression ◽  
Mrna Level ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Cycle Progression ◽  
Arterial Smooth Muscle Cells ◽  
Cycle Dependent

Because exogenous ATP is suspected to influence the proliferative process, its effects on the cell cycle progression of arterial smooth muscle cells were studied by investigating changes in the mRNA steady-state level of cell cycle-dependent genes. Stimulation of cultured quiescent smooth muscle cells by exogenous ATP induced chronological activation not only of immediate-early but also of delayed-early cell cycle-dependent genes, which were usually expressed after a mitogenic stimulation. In contrast, ATP did not increase late G1 gene mRNA level, demonstrating that this nucleotide induces a limited cell cycle progression of arterial smooth muscle cells through the G1 phase but is not able by itself to induce crossing over the G1-S boundary and consequently DNA synthesis. An increase in c-fos mRNA level was also induced by ADP but not by AMP or adenosine. Moreover, 2-methylthioadenosine 5'-triphosphate but not alpha, beta-methyleneadenosine 5'-triphosphate mediated this kind of response. Taken together, these results demonstrate that extracellular ATP induces the limited progression of arterial smooth muscle cells through the G1 phase via its fixation on P2 gamma receptors.

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