NDLI: Cholera toxin treatment of vascular smooth muscle cells decreases smooth muscle α-actin content and abolishes the platelet-derived growth factor-BB-stimulated DNA synthesis

Content Provider	PubMed Central
Author	Sachinidis, Agapios Seul, Claudia Gouni-berthold, Ioanna Seewald, Stefan Ko, Yon Vetter, Hans Fingerle, Jürgen Hoppe, Jürgen
Copyright Year	2000
Abstract	The second messenger cyclic AMP regulates diverse biological processes such as cell morphology and cell growth. We examined the role of the second messenger cyclic AMP on rat aortic vascular smooth muscle cell (VSMC) morphology and the intracellular transduction pathway mediated by platelet-derived growth factor β-receptor (PDGF-Rβ). The effect of PDGF-BB on VSMCs growth was assessed by [3H]-thymidine incorporation. Tyrosine phosphorylation of PDGF-Rβ, PLC-γ1, ERK1 and ERK2, p125FAK and paxillin as well as Sm α-actin was examined by the chemiluminescence Western blotting method. Actin mRNA level was quantitated by Northern blotting. Visualization of Sm α-actin filaments, paxillin and PDGF-Rβ was performed by immunfluorescence microscopy. Cholera toxin (CTX; 10 nM) treatment lead to a large and sustained increase in the cyclic AMP concentration after 2 h which correlated with change of VSMC morphology including complete disruption of the Sm α-actin filament array and loss of focal adhesions. Treatment of VSMCs with CTX did not influence tyrosine phosphorylation of p125FAK and paxillin but decreased the content of a Sm α-actin protein. Maximal decrease of 70% was observed after 24 h of treatment. CTX also caused a 90% decrease of the actin mRNA level. CTX treatment completely abolished PDGF-BB stimulated DNA-synthesis although PDGF-Rβ level and subcellular distribution and translocation was not altered. Furthermore CTX attenuated the PDGF-BB-induced tyrosine phosphorylation of the PDGF-Rβ, PI 3′-K, PLC-γ1 and ERK1/2 indicating an action of cyclic AMP on PDGF-β receptor. We conclude that although cyclic AMP attenuates the PDGF-Rβ mediated intracellular transduction pathway, an intact actin filament may be required for the PDGF-BB-induced DNA synthesis in VSMCs.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0703480
Ending Page	1570
Page Count	10
Starting Page	1561
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	7
Volume Number	130
Language	English
Publisher Date	2000-08-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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