A Novel 31-Amino-Acid-Length Endothelin, ET-1(1–31), Can Act as a Biologically Active Peptide for Vascular Smooth Muscle Cells

2000 ◽  
Vol 275 (2) ◽  
pp. 595-600 ◽  
Author(s):  
Noriko Nagata ◽  
Yasuharu Niwa ◽  
Yutaka Nakaya
Keyword(s):  
Smooth Muscle ◽  
Amino Acid ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Biologically Active ◽  
Active Peptide ◽  
Amino Acid Length ◽  
Biologically Active Peptide

Insulin Signaling and Its Regulation of System A Amino Acid Uptake in Cultured Rat Vascular Smooth Muscle Cells

1996 ◽  
Vol 79 (6) ◽  
pp. 1167-1176 ◽  
Author(s):  
Toshiyuki Obata ◽  
Atsunori Kashiwagi ◽  
Hiroshi Maegawa ◽  
Yoshihiko Nishio ◽  
Satoshi Ugi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Amino Acid ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Insulin Signaling ◽  
Muscle Cells ◽  
Amino Acid Uptake ◽  
Acid Uptake ◽  
System A

scholarly journals 1-O-alkyl-2-acetyl-sn-glycerol: a platelet-activating factor metabolite with biological activity in vascular smooth muscle cells.

1989 ◽  
Vol 1 (1) ◽  
pp. 13-25 ◽  
Author(s):  
L L Stoll ◽  
P H Figard ◽  
N R Yerram ◽  
M A Yorek ◽  
A A Spector
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Platelet Activating Factor ◽  
Ether Lipid ◽  
Muscle Cells ◽  
Biologically Active ◽  
Vitro Assay

Platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine; PAF) is a potent vasoactive ether lipid produced by activated blood cells and endothelial cells. Vascular smooth muscle cells partially convert exogenous PAF to 1-O-alkyl-2-acetyl-sn-glycerol (AAG), a biologically active diacylglycerol analogue. AAG is formed rapidly (less than 15 s) after exposure of the smooth muscle cells and does not appear to be a substrate for diacylglycerol kinase in these cells. Although most of the compound is metabolized to 1-O-alkyl-sn-glycerol, a small quantity remains as AAG for greater than or equal to 6 h. AAG inhibits phorbol ester binding, and it is as effective an activator of protein kinase C as diolein in an in vitro assay. Furthermore, AAG and PAF produce the same pattern of effects on smooth muscle cell proliferation. These observations suggest that at least some of the actions of PAF in vascular smooth muscle may be mediated through the formation of AAG, a stable, bioactive metabolite that appears to function as a diacylglycerol analogue.

Multiple growth factors are released from mechanically injured vascular smooth muscle cells

1995 ◽  
Vol 269 (5) ◽  
pp. H1641-H1647 ◽  
Author(s):  
S. T. Crowley ◽  
C. J. Ray ◽  
D. Nawaz ◽  
R. A. Majack ◽  
L. D. Horwitz
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Conditioned Medium ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mitogenic Activity ◽  
Biologically Active

Local release of mitogenic and chemotactic signals during angioplasty-induced vascular injury may initiate restenosis. We investigated whether mechanical injury to vascular smooth muscle cells (VSMC) results in the release of biologically active peptide growth factors. Monolayers of bovine SMC cultures were mechanically injured by cell scraping. Conditioned medium (CM) from control and injured SMC cultures was collected, and the mitogenic activity was measured by [3H]thymidine incorporation in recipient SMC cultures. Mitogenic activity from injured CM was detected within 15 min after injury. When the CM from injured cells was removed 15 min after injury and replaced with serum-free media, there was no detectable mitogenic activity in the replacement CM assessed 1-6 days postinjury. Suramin, a nonspecific peptide growth factor antagonist, significantly inhibited the mitogenic activity of injured CM. Basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF A chain), and epidermal growth factor (EGF) were detected in CM from injured cells by immunoblot analysis. The mitogenic activity of injured CM was significantly inhibited with neutralizing antibodies to bFGF (34%), PDGF-AA (32%), PDGF-BB (25%), and EGF (25%). A neutralizing antibody to transforming growth factor (TGF)-beta had no effect. In conclusion, bFGF, PDGF, and EGF are immediately released from mechanically injured VSMC. VSMC likely contain preformed, biologically active growth factors that are efficiently released from the cell cytoplasm following mechanical injury. Conditioned medium from injured VSMC is highly mitogenic, and this activity is probably due to multiple growth factors interacting synergistically.

scholarly journals Regulatory effects of 1,25-dihydroxyvitamin D3 on vascular smooth muscle cells.

2012 ◽  
Vol 59 (3) ◽  
Author(s):  
Stefan Tukaj ◽  
Piotr Trzonkowski ◽  
Cecylia Tukaj
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Biologically Active ◽  
Central Feature ◽  
Anti Inflammatory ◽  
Regulatory Effects

Inflammatory response has been recognized as a central feature in the development and progression of atherosclerosis, and VSMCs (Vascular Smooth Muscle Cells) - the main cellular component of media, play an important role in this process. Many reports indicate that the biologically active vitamin D metabolite - 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3) = calcitriol), besides its well established role in calcium homeostasis, plays an essential role in the regulation of the inflammation process. The aim of this study was to determine the regulatory effects of calcitriol, applied at two supra-physiological doses (10 nM and 100 nM), in VSMC culture. Secretion of the pro-inflammatory cytokines, IL-6 and TNF-α, was significantly attenuated in calcitriol-treated VSMC culture, but the level of anti-inflammatory TGF-β was generally unchanged. Since in advanced atherosclerosis lesions several cell types, including VSMCs, overproduce the HSP70 chaperone protein, we also checked the effects of calcitriol on its synthesis. The presence of 1,25(OH)(2)D(3) did not affect HSP70 synthesis under physiological conditions but the synthesis of HSP70 in VSMCs exposed to heat shock was significantly inhibited by calcitriol (=100 nM). We observed that 1,25(OH)(2)D(3) induced SOD 1 activity, stimulated the expression of IκB-α, and did not influence the level of NF-κB-p65 in VSMCs. The results of our study suggest that 1,25(OH)(2)D(3) may serve as a natural anti-inflammatory agent and may therefore play a beneficial role in the physiology of VSMC in some contexts of atherosclerosis.

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