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Titolo:
Signal transduction in smooth muscle - Invited review: cGMP-dependent protein kinase signaling mechanisms in smooth muscle: from the regulation of tone to gene expression
Autore:
Lincoln, TM; Dey, N; Sellak, H;
Indirizzi:
Univ Alabama, Dept Pathol, Div Mol & Cellular Pathol, Birmingham, AL 35294USA Univ Alabama Birmingham AL USA 35294 ular Pathol, Birmingham, AL 35294USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 3, volume: 91, anno: 2001,
pagine: 1421 - 1430
SICI:
8750-7587(200109)91:3<1421:STISM->2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; SHOCK-RELATED PROTEIN; VASODILATOR-STIMULATED PHOSPHOPROTEIN; HUMAN ATHEROSCLEROTIC LESIONS; LIGHT-CHAIN PHOSPHATASE; SWINE CAROTID-ARTERY; CYCLIC-GMP PATHWAY; FOCAL ADHESION; RAT AORTA;
Keywords:
vascular smooth muscle cells; nitric oxide;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
117
Recensione:
Indirizzi per estratti:
Indirizzo: Lincoln, TM Univ Alabama, Dept Pathol, Div Mol & Cellular Pathol, Birmingham, AL 35294USA Univ Alabama Birmingham AL USA 35294 Birmingham, AL 35294USA
Citazione:
T.M. Lincoln et al., "Signal transduction in smooth muscle - Invited review: cGMP-dependent protein kinase signaling mechanisms in smooth muscle: from the regulation of tone to gene expression", J APP PHYSL, 91(3), 2001, pp. 1421-1430

Abstract

cGMP is a second messenger that produces its effects by interacting with intracellular receptor proteins. In smooth muscle cells, one of the major receptors for cGMP is the serine/threonine protein kinase, cGMP-dependent protein kinase (PKG). PKG has been shown to catalyze the phosphorylation of a number of physiologically relevant proteins whose function it is to regulate the contractile activity of the smooth muscle cell. These include proteins that regulate free intracellular calcium levels, the cytoskeleton, and the phosphorylation state of the regulatory light chain of smooth muscle myosin. Other studies have shown that vascular smooth muscle cells (VSMCs) thatare cultured in vitro may cease to express PKG and will, coincidentally, acquire a noncontractile, synthetic phenotype. The restoration of PKG expression to the synthetic phenotype VSMC results in the cells acquiring a more contractile phenotype. These more recent studies suggest that PKG controls VSMC gene expression that, in turn, regulates phenotypic modulation of the cells. Therefore, the regulation of PKG gene expression appears to be linked to phenotypic modulation of VSMC. Because several vascular disorders are related to the accumulation of synthetic, fibroproliferative VSMC in the vessel wall, it is likely that changes in the activity of the nitric oxide/cGMP/PKG pathway is involved the development of these diseases.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/21 alle ore 02:55:30