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    188宝金博页面版: Regulation of PKG expression in vascular smooth muscle cells

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    内容提示： BioMed CentralPage 1 of 1(page number not for citation purposes)BMC PharmacologyOpen AccessOral presentationRegulation of PKG expression in vascular smooth muscle cellsYing Zeng and Renate B Pilz*Address: University of California at San Diego, USAEmail: Renate B Pilz* - rpilz@ucsd.edu* Corresponding author Type I cGMP-dependent protein kinase (PKG I) plays amajor role in vascular homeostasis mediating smoothmuscle relaxation in response to nitric oxide, but rela-tively little is known about the regulati...

    文档格式：PDF | 页数：1 | 浏览次数：43 | 上传日期：2015-11-18 09:09:33 | 文档星级：
    BioMed CentralPage 1 of 1(page number not for citation purposes)BMC PharmacologyOpen AccessOral presentationRegulation of PKG expression in vascular smooth muscle cellsYing Zeng and Renate B Pilz*Address: University of California at San Diego, USAEmail: Renate B Pilz* - rpilz@ucsd.edu* Corresponding author Type I cGMP-dependent protein kinase (PKG I) plays amajor role in vascular homeostasis mediating smoothmuscle relaxation in response to nitric oxide, but rela-tively little is known about the regulation of PKG I expres-sion. Rho family GTPases (including RhoA and Rac1) areregulated by growth factors and cell adhesion moleculesand modulate cell proliferation and motility as well asgene expression. We found opposing effects of RhoA andRac1 on PKG I expression: (i) cell density-inducedincreases in PKG I expression occurred under conditionsof high Rac1 activity and low RhoA activity in post-conflu-ent cells; (ii) activation of RhoA by calpeptin suppressedPKG I, whereas down-regulation of RhoA by siRNAincreased PKG I expression; and (iii) PKG I promoteractivity was suppressed in cells expressing active RhoA orRho-kinase, but was enhanced in cells expressing activeRac1, a dominant negative RhoA, or p120 catenin. Sp1consensus sequences in the PKG I promoter were requiredfor Rho regulation and bound nuclear proteins in a celldensity-dependent manner, including the Krüppel-likefactor 4 (KLF4). KLF4 was identified as the major trans-acting factor at two proximal SP1 sites; active RhoA sup-pressed KLF4 DNA binding and transactivation potentialon the PKG I promoter. We propose a novel mechanismfor cell density-dependent regulation of gene expressioninvolving Rho and Rac; moreover, suppression of PKG Iexpression by RhoA may explain the decrease in vascularsmooth muscle cell PKG I levels found in some models ofhypertension and vascular injury.from 2nd International Conference of cGMP Generators, Effectors and Therapeutic ImplicationsPotsdam, Germany, 10–12 June, 2005Published: 16 June 2005BMC Pharmacology 2005, 5(Suppl 1):S16doi:10.1186/1471-2210-5-S1-S16

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