Dissociation of vasoconstrictor-stimulated basic fibroblast growth factor expression from hypertrophic growth in cultured vascular smooth muscle cells. Relevant roles of protein kinase C.

@article{Ali1994DissociationOV,
  title={Dissociation of vasoconstrictor-stimulated basic fibroblast growth factor expression from hypertrophic growth in cultured vascular smooth muscle cells. Relevant roles of protein kinase C.},
  author={S. Ali and Michael W. Becker and M. G. Davis and Gerald W. Dorn},
  journal={Circulation research},
  year={1994},
  volume={75 5},
  pages={
          836-43
        }
}
Thromboxane A2 (TXA2) and angiotensin II (Ang II) stimulate vascular smooth muscle hypertrophy by upregulating endogenous synthesis of basic fibroblast growth factor (bFGF). Because mitogenic phorbol esters can also stimulate bFGF formation, we investigated the role of protein kinase C (PKC) in vascular smooth muscle cell (VSMC) bFGF formation and hypertrophy. Preliminary characterization of PKC isoform expression in VSMC by use of polymerase chain reaction identified PKC alpha, delta, epsilon… 
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Thromboxane/prostaglandin endoperoxide-induced hypertrophy of rat vascular smooth muscle cells is signaled by protein kinase C-dependent increases in transforming growth factor-beta.
TLDR
Results of the present study suggest that TGF-beta and bFGF interact in mediating the protein synthetic response to U46619, and demonstrate that thromboxane/prostaglandin endoperoxide signals increased T GF-beta bioactivity via protein kinase C.
The role of protein kinase C in activation and termination of mitogen-activated protein kinase activity in angiotensin II-stimulated rat aortic smooth-muscle cells.
Differential effects of protein kinase C on human vascular smooth muscle cell proliferation and migration.
TLDR
It is found that PKC activation enhances proliferation but inhibits migration of human vascular SMC, and these differential effect of PKC on vascular cells appears to be mediated through PKC-alpha, -beta I, -delta, and/or -epsilon.
Glycated serum albumin-induced vascular smooth muscle cell proliferation through activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway by protein kinase C.
TLDR
It is shown that the MAPK cascade is required for GSA-induced proliferation, and that phorbol ester-sensitive PKC isoforms contribute to cell activation and proliferation in GSA -stimulated VSMC.
Angiotensin II and endothelin-1 increase fibroblast growth factor-2 mRNA expression in vascular smooth muscle cells.
TLDR
It is reported that Ang II treatment of rat aortic SMC increases fibroblast growth factor-2 (FGF-2) but not FGF-1 mRNA levels, indicating that F GF-2 gene expression is up-regulated by two distinct vasoactive peptides implicated in vascular SMC growth control in vivo.
Rapid activation of the novel serine/threonine protein kinase, protein kinase D by phorbol esters, angiotensin II and PDGF‐BB in vascular smooth muscle cells
Overexpression of protein kinase Cα enhances lipopolysaccharide‐induced nitric oxide formation in vascular smooth muscle cells
TLDR
It is suggested that PKCα plays an important role in LPS‐induced NO formation and that a significant portion of this effect may be by means of enhanced substrate availability to the inducible nitric oxide synthase enzyme.
Induction of basic fibroblast growth factor mRNA by basic fibroblast growth factor in Müller cells.
TLDR
Investigation of the induction of basic fibroblast growth factor (bFGF) gene expression in cultured rat Müller cells by bFGF and the mechanism of induction indicate that b FGF induces bF GF gene expression through PKC activation, which raises the possibility that Müllers cells in vivo also respond to available bFGI or to exogenous bFGR by producing more bFFGF, which could in turn promote photoreceptor survival.
Prostaglandin D2 inhibits inducible nitric oxide synthase expression in rat vascular smooth muscle cells.
TLDR
The data suggest that PGD2 suppresses NO generation in VSMCs by inhibiting iNOS mRNA expression, most likely through the cascade of the PGJ2 series rather than through the TX receptor or cAMP upregulation.
Protein kinase C-α regulates proliferation but not apoptosis in rat coronary vascular smooth muscle cells
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References

SHOWING 1-10 OF 33 REFERENCES
Thromboxane A2 stimulates vascular smooth muscle hypertrophy by up-regulating the synthesis and release of endogenous basic fibroblast growth factor.
TLDR
Results indicate that increased expression and release of endogenous bFGF, but not direct tyrosine phosphorylation, mediates the hypertrophic vascular smooth muscle response to thromboxane.
Dissociation of the contractile and hypertrophic effects of vasoconstrictor prostanoids in vascular smooth muscle.
Multiple autocrine growth factors modulate vascular smooth muscle cell growth response to angiotensin II.
TLDR
It is demonstrated that in these VSMC, TGF-beta 1 affects a key antiproliferative action, modulating the mitogenic properties of bFGF, a potent mitogen for VSMC.
Protein kinase C-mediated inhibition of vascular smooth muscle cell proliferation: the isoforms that may mediate G1/S inhibition.
TLDR
KPC-alpha and -epsilon may be the most probable mediators of the G1/S inhibition of vascular smooth muscle cell proliferation.
Angiotensin II induces c-fos mRNA in aortic smooth muscle. Role of Ca2+ mobilization and protein kinase C activation.
TLDR
Results demonstrate that the vasoconstrictor hormone Ang II induces in VSMC one of the earliest genes, c-fos, associated with the proliferative response.
Bombesin, platelet-derived growth factor, and diacylglycerol induce selective membrane association and down-regulation of protein kinase C isotypes in Swiss 3T3 cells.
Protein kinase C activation allows pulmonary artery smooth muscle cells to proliferate to hypoxia.
TLDR
Pulmonary artery (PA) smooth muscle cell (SMC) proliferation occurs with hypoxic pulmonary hypertension in vivo and the PMA-primed cells seemed to "acquire" the ability to directly sense hypoxia and proliferate, suggesting activation of PKC may be a requisite step for PA SMC to respond directly to hypoxIA.
Effect of TPA on ion fluxes and DNA synthesis in vascular smooth muscle cells
TLDR
The findings suggest that the inhibitory effect of TPA on EGF-receptor functions goes beyond previously reported effects on Na/H exchange in A431 cells and extends to E GF-stimulation of Na/K/Cl co- transport and DNA synthesis in vascular smooth muscle cells.
Thromboxane A2 stimulated signal transduction in vascular smooth muscle.
  • G. Dorn, M. Becker
  • Biology, Chemistry
    The Journal of pharmacology and experimental therapeutics
  • 1993
TLDR
It is suggested that agonist occupation of TXA2 receptors produces vascular smooth muscle contraction through initial activation of phospholipase C with production of 1,4,5-inositol phosphate, release of intracellular calcium stores and phosphorylation of myosin light chains associated with cellular acidification, presumably via activation of Ca++ ATPase.
Cultured human vascular smooth muscle cells with functional thromboxane A2 receptors: measurement of U46619-induced 45calcium efflux.
TLDR
The results suggest that the effects of U46619 in increasing vascular smooth muscle cell calcium efflux are receptor mediated, and vascular smooth Muscle cells with functional TXA2/PGH2 receptors were cultured from human saphenous veins and provide a potentially useful in vitro system for the further study of TXA 2/ PGH2 receptor-mediated phenomena in human vascular tissue.
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