Extracellular mechanism through the Edg family of receptors might be responsible for sphingosine-1-phosphate-induced regulation of DNA synthesis and migration of rat aortic smooth-muscle cells

2001 ◽  
Vol 353 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Ken-ichi TAMAMA ◽  
Junko KON ◽  
Koichi SATO ◽  
Hideaki TOMURA ◽  
Atsushi KUWABARA ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Sphingosine 1 Phosphate ◽  
And Migration

scholarly journals Studies on sporadic non-syndromic thoracic aortic aneurysms: 1. Deregulation of Jagged/Notch 1 homeostasis and selection of synthetic/secretor phenotype smooth muscle cells

2018 ◽  
Vol 25 (1_suppl) ◽  
pp. 42-50 ◽  
Author(s):  
Anna Chiarini ◽  
Francesco Onorati ◽  
Maddalena Marconi ◽  
Alessandra Pasquali ◽  
Cristina Patuzzo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Muscle Cells ◽  
Aortic Aneurysms ◽  
Aortic Smooth Muscle Cells ◽  
Thoracic Aortic Aneurysms ◽  
Aortic Smooth Muscle ◽  
And Migration ◽  
Media Layer

Background Sporadic non-syndromic thoracic aortic aneurysms (SNSTAAs) are less well understood than familial non-syndromic or syndromic ones. The study aimed at defining the peculiar morphologic and molecular changes occurring in the media layer of SNSTAAs. Design This study was based on a single centre design. Methods Media layer samples taken from seven carefully selected SNSTAAs and seven reference patients (controls) were investigated via quantitative polymerase chain reaction, proteomics-bioinformatics, immunoblotting, quantitative histology, and immunohistochemistry/immunofluorescence. Results In SNSTAAs media, aortic smooth muscle cells numbers were halved due to an apoptotic process coupled with a negligible cell proliferation. Cystathionine γ-lyase was diffusely up-regulated. Surviving aortic smooth muscle cells exhibited diverging phenotypes: in inner- and outer-media contractile cells prevailed, having higher contents of smooth-muscle-α-actin holoprotein (45-kDa) and of caspase-3-cleaved smooth-muscle-α-actin 25-kDa fragments; in mid-media, aortic smooth muscle cells exhibited a synthetic/secretor phenotype, down-regulating vimentin, but up-regulating glial fibrillary acidic protein, trans-Golgi network 46 protein, Jagged1 (172-kDa) holoprotein, and Jagged1’s receptor Notch1. Extracellular soluble Jagged1 (42-kDa) fragments accumulated. Conclusions In SNSTAAs, there is a relentless aortic smooth muscle cells attrition caused by the up-regulated cystathionine γ-lyase. In mid-media, synthetic/secretor aortic smooth muscle cells intensify Jagged1/NOTCH1 signalling in the attempt to counterbalance the weakened aortic wall, due to aortic smooth muscle cells net loss and mechanical stress. Synthetic/secretor aortic smooth muscle cells are apoptosis-prone, and the accruing thrombin-cleaved Jagged1 fragments counteract the otherwise useful effects of Jagged1/NOTCH1 signalling, thus hampering tissue homeostasis/remodelling, and aortic smooth muscle cells adhesion, differentiation, and migration.

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.

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