Picture of UK Houses of Parliament

Leading national thinking on politics, government & public policy through Open Access research

Strathprints makes available scholarly Open Access content by researchers in the School of Government & Public Policy, based within the Faculty of Humanities & Social Sciences.

Research here is 1st in Scotland for research intensity and spans a wide range of domains. The Department of Politics demonstrates expertise in understanding parties, elections and public opinion, with additional emphases on political economy, institutions and international relations. This international angle is reflected in the European Policies Research Centre (EPRC) which conducts comparative research on public policy. Meanwhile, the Centre for Energy Policy provides independent expertise on energy, working across multidisciplinary groups to shape policy for a low carbon economy.

Explore the Open Access research of the School of Government & Public Policy. Or explore all of Strathclyde's Open Access research...

PDGF-induced signaling in proliferating and differentiated vascular smooth muscle: effects of altered intracellular Ca2+ regulation

Egan, C. and Wainwright, C.L. and Wadsworth, R. and Nixon, G.F. (2005) PDGF-induced signaling in proliferating and differentiated vascular smooth muscle: effects of altered intracellular Ca2+ regulation. Cardiovascular Research, 67 (2). pp. 308-316. ISSN 0008-6363

Full text not available in this repository.Request a copy from the Strathclyde author

Abstract

Objective: Platelet-derived growth factor-BB (PDGF)-induced intracellular signaling is involved in phenotypic modulation of vascular smooth muscle (VSM). This study has examined the PDGF-induced Ca2+ increase and the resultant effect on signaling pathways in proliferative compared with fully differentiated VSM. Methods: PDGF-induced changes in Ca2+ were measured in portal vein (PV) myocytes from 2–4-day-old (proliferating), compared to 6-week-old (differentiated), Sprague Dawley rats. Phospholipase C (PLC)g expression and activation of extracellular signal-regulated kinase (ERK) 1/2 was determined by immunoblotting or confocal immunolabelling. Activation of the Ca2+-dependent transcription factor, nuclear factor of activated T-cells (NFATc), was assessed by electromobility shift assay. Results: PDGF increased the intracellular Ca2+ concentration in differentiated, but not in proliferating, PV myocytes. This is probably due to very low expression of PLCg in proliferating PV. In 6-week-old PV, PDGF stimulation induced nuclear translocation and activation of NFATc. PDGF did not induce NFATc activation in neonatal PV. PDGF-induced ERK1/2 activation was observed in both 2–4-day-old and 6-week-old PV. In 6-week-old PV, ERK1/2 activation was Ca2+-dependent and protein kinase C-dependent. However in 2–4-day-old PV, PDGF-induced ERK1/2 activation was via a Ca2+-independent, atypical protein kinase C. PLCg expression was also decreased in the neointima, compared to media, of balloon-injured rabbit subclavian arteries. Conclusions: The regulation of PDGF-induced Ca2+ increases by PLCg expression in VSM may provide a mechanism for coordinating different signaling pathways leading to activation of specific transcription factors. This may play an important role in the phenotypic modulation of VSM.