scholarly journals Prostaglandin E2 Inhibits Histamine-Evoked Ca2+ Release in Human Aortic Smooth Muscle Cells through Hyperactive cAMP Signaling Junctions and Protein Kinase A

2017 ◽  
Vol 92 (5) ◽  
pp. 533-545 ◽  
Author(s):  
Emily J. A. Taylor ◽  
Evangelia Pantazaka ◽  
Kathryn L. Shelley ◽  
Colin W. Taylor
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Prostaglandin E2 ◽  
Protein Kinase A ◽  
Muscle Cells ◽  
Camp Signaling ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Kinase A

Antiproliferative action of protein kinase C in cultured rabbit aortic smooth muscle cells

1987 ◽  
Vol 173 (2) ◽  
pp. 504-514 ◽  
Author(s):  
Ken-Ichi Kariya ◽  
Yasuo Fukumoto ◽  
Terutaka Tsuda ◽  
Takeshi Yamamoto ◽  
Yasuhiro Kawahara ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Kinase C ◽  
Antiproliferative Action

Regulation of prostacyclin production by [Ca2+]i and protein kinase C in aortic smooth muscle cells

1992 ◽  
Vol 263 (4) ◽  
pp. E800-E806
Author(s):  
A. C. Erbrich ◽  
D. J. Church ◽  
M. B. Vallotton ◽  
U. Lang
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Prolonged Incubation ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Kinase C ◽  
Prostacyclin Production

The respective roles of protein kinase C (PKC) and of cytosolic free Ca2+ concentration ([Ca2+]i) in prostacyclin synthesis were investigated in aortic smooth muscle cells by using A23187 and phorbol 12-myristate 13-acetate (PMA) to bypass the hormonal receptor. Exposure of the cells to A23187 markedly increased prostacyclin production, which was not affected by the PKC inhibitor staurosporine or by PKC depletion after prolonged incubation (48 h) of cells with PMA. The increase in [Ca2+]i induced by A23187 did not affect membranous or cytosolic PKC activity in control and PMA-stimulated cells. Activation of PKC by PMA, a weak stimulant of prostacyclin production by itself, strongly potentiated A23187-induced prostacyclin production, as well as that induced by the calcium-mobilizing hormone arginine vasopressin (AVP). The potentiating effect persisted for 30 min after the removal of PMA. However, this "memory" effect was not due to sustained levels of membranous PKC activity but probably to the prolonged influence of PKC-induced phosphorylation(s). Taken together, our results suggest that, although an increase in [Ca2+]i is sufficient for inducing prostacyclin production in rat aortic smooth muscle cells, activation of PKC is necessary for AVP-induced prostacyclin production in this same tissue.

Antimitogenic Effects of Trapidil In Coronary Artery Smooth Muscle Cells by Direct Activation of Protein Kinase A

1998 ◽  
Vol 54 (2) ◽  
pp. 241-248 ◽  
Author(s):  
Detlef Bönisch ◽  
Artur-Aron Weber ◽  
Michael Wittpoth ◽  
Michael Osinski ◽  
Karsten Schrör
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Protein Kinase A ◽  
Muscle Cells ◽  
Direct Activation ◽  
Kinase A

Phospholipase C and adenylate cyclase signalling systems in the action of hCG on porcine myometrial smooth muscle cells

1996 ◽  
Vol 148 (1) ◽  
pp. 175-180 ◽  
Author(s):  
J Kisielewska ◽  
A P F Flint ◽  
A J Ziecik
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Protein Kinase A ◽  
Muscle Cells ◽  
Target Tissue ◽  
Myometrial Cells ◽  
Kinase C ◽  
Kinase A

Abstract Although the uterus is a target tissue for LH and its homologue hCG the second messenger system responding to LH/hCG in myometrial cells is not established. In this study we investigated the involvement of protein kinase A and protein kinase C in the action of hCG on porcine myometrial smooth muscle cells in vitro. Myometrium was obtained from ovariectomized gilts given 2·5 mg oestradiol benzoate plus 50 mg progesterone for five consecutive days. Myometrial cells were cultured for 48 h and different doses of hCG were then added. Increasing doses of hCG stimulated concentration-dependent increases in [3H]inositol phosphates (IPs) accumulation in incubations lasting 24 h. The highest dose of hCG (1000 mU/ml) increased turnover of IPs by 2·4-fold as reflected in elevations in IP1, IP2 and IP3, and similar effects were observed with noradrenaline. The time- and concentration-dependent effects of hCG on IPs accumulation occurred between 16 and 24 h of incubation. Incubation of myocytes with the lowest doses of hCG (0·1 and 1 mU/ml) caused a significant increase in cAMP accumulation but the highest doses (10–1000 mU/ml) had no effect on cAMP concentrations. This is the first demonstration that LH/hCG receptor signalling leads to increased inositol phosphate turnover in myometrial cells as well as cAMP generation and it leads to the conclusion that both protein kinase A and protein kinase C signalling mechanisms are involved in gonadotrophin action in porcine myometrial smooth muscle cells. Journal of Endocrinology (1996) 148, 175–180

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