Effect of pituitary adenylate cyclase activating polypeptide on vasopressin-induced proliferation of aortic smooth muscle cells: comparison with vasoactive intestinal polypeptide

1993 ◽  
Vol 71 (3-4) ◽  
pp. 156-161 ◽  
Author(s):  
Yutaka Oiso ◽  
Jun Kotoyori ◽  
Takashi Murase ◽  
Yoshiaki Ito ◽  
Osamu Kozawa
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
Adenylate Cyclase ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Vasoactive Intestinal Polypeptide ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Pituitary Adenylate Cyclase

Pituitary adenylate cyclase activating polypeptide (PACAP) inhibited dose dependently the DNA synthesis stimulated by arginine vasopressin (AVP) in cultured rat aortic smooth muscle cells (SMC). The inhibition was cell cycle dependent and the maximum inhibition was observed when added at the late G1 phase of the cell cycle. Vasoactive intestinal polypeptide (VIP), which shows a considerable homology with PACAP, also inhibited dose dependently the AVP-induced DNA synthesis in a cell cycle dependent manner. The maximum inhibition was also observed at the late G1 phase. The patterns of both the dose-dependent inhibitions were similar, and the inhibition by a combination of PACAP and VIP was not additive. PACAP stimulated dose dependently cAMP accumulation in aortic SMC. VIP also stimulated cAMP accumulation, and the accumulation by a combination of PACAP and VIP was not additive. Both PACAP and VIP had little effect on phosphoinositide hydrolysis in these cells. The suppression of the AVP-induced DNA synthesis by PACAP or VIP was enhanced by 3-isobutyl-1-methylxanthine, an inhibitor for phosphodiesterases. Dibutyryl cAMP, but not 8-bromo-cGMP, inhibited the AVP-induced DNA synthesis, and a combination of PACAP and dibutyryl cAMP was not additive. [Ac-Tyr1, D-Phe2]growth hormone-releasing factor, an antagonist for VIP receptor, reversed the inhibitory effect of PACAP on the AVP-induced DNA synthesis. These results suggest that PACAP has an antiproliferative effect on aortic SMC at the late G1 phase of the cell cycle through cAMP production, and that PACAP and VIP inhibit the AVP-induced DNA synthesis by a common mechanism.Key words: pituitary adenylate cyclase activating polypeptide, vasoactive intestinal polypeptide, arginine vasopressin, DNA synthesis, aortic smooth muscle cells.

scholarly journals Transforming growth factor-beta-induced growth inhibition and cellular hypertrophy in cultured vascular smooth muscle cells.

1988 ◽  
Vol 107 (2) ◽  
pp. 771-780 ◽  
Author(s):  
G K Owens ◽  
A A Geisterfer ◽  
Y W Yang ◽  
A Komoriya
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Tgf Beta ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Cellular Hypertrophy

We have explored the hypothesis that hypertrophy of vascular smooth muscle cells may be regulated, in part, by growth inhibitory factors that alter the pattern of the growth response to serum mitogens by characterizing the effects of the potent growth inhibitor, transforming growth factor-beta (TGF-beta), on both hyperplastic and hypertrophic growth of cultured rat aortic smooth muscle cells. TGF-beta inhibited serum-induced proliferation of rat aortic smooth muscle cells (ED50 = 2 pM); this is consistent with previously reported observations in bovine aortic smooth muscle cells (Assoian et al. 1982. J. Biol. Chem. 258:7155-7160). Growth inhibition was due in part to a greater than twofold increase in the cell cycle transit time in cells that continued to proliferate in the presence of TGF-beta. TGF-beta concurrently induced cellular hypertrophy as assessed by flow cytometric analysis of cellular protein content (47% increase) and forward angle light scatter (32-50% increase), an index of cell size. In addition to being time and concentration dependent, this hypertrophy was reversible. Simultaneous flow cytometric evaluation of forward angle light scatter and cellular DNA content demonstrated that TGF-beta-induced hypertrophy was not dependent on withdrawal of cells from the cell cycle nor was it dependent on growth arrest of cells at a particular point in the cell cycle in that both cycling cells in the G2 phase of the cell cycle and those in G1 were hypertrophied with respect to the corresponding cells in vehicle-treated controls. Chronic treatment with TGF-beta (100 pM, 9 d) was associated with accumulation of cells in the G2 phase of the cell cycle in the virtual absence of cells in S phase, whereas subsequent removal of TGF-beta from these cultures was associated with the appearance of a significant fraction of cycling cells with greater than 4c DNA content, consistent with development of tetraploidy. Results of these studies support a role for TGF-beta in the control of smooth muscle cell growth and suggest that at least one mechanism whereby hypertrophy and hyperploidy may occur in this, as well as other cell types, is by alterations in the response to serum mitogens by potent growth inhibitors such as TGF-beta.

scholarly journals Cholesterol Enhances Platelet-Derived Growth Factor-BB-Induced [Ca 2+ ] i and DNA Synthesis in Rat Aortic Smooth Muscle Cells

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 326-333 ◽  
Author(s):  
Agapios Sachinidis ◽  
Min Liu ◽  
Artur-Aron Weber ◽  
Claudia Seul ◽  
Volker Harth ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

scholarly journals The effect of anti-hypertensive drugs on DNA synthesis and proliferation of ultured rat aortic smooth muscle cells

1997 ◽  
Vol 38 (3) ◽  
pp. 160
Author(s):  
Shin Wook Kang ◽  
In Hee Lee ◽  
Kyu Hun Choi ◽  
Ho Yung Lee ◽  
Dae Suk Han
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle
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