title: PDGF-induced proliferation of smooth muscular cells is related to the regulation of CREB phosphorylation and Nur77 expression.
abstract: This study examined the relationship between PDGF-induced proliferation of vascular smooth muscle cells (VSMCs) and Nur77 expression and the effect of atorvastatin on VSMC proliferation and Nur77 in PDGF-treated VSMCs. Rat VSMCs were isolated and cultured. After incubation with atorvastatin or Nur77 siRNA, the cells were stimulated with PDGF and detected for BrdU incorporation to measure the proliferation of the VSMCs. Quantitative PCR and Western blotting were used to determine the Nur77 protein and the CREB phosphorylation level, to observe their relations with PDGF-induced VSMC proliferation. Our results showed that PDGF increased the BrdU incorporation in VSMCs, suggesting that it induced the proliferation of the cells. The VSMC proliferation was associated with increased Nur77 expression and elevated CREB phosphorylation. Atorvastatin inhibited the PDGF-induced VSMC proliferation, suppressed Nur77 expression. After silencing of Nur77 gene, the PDGF-induced VSMC proliferation was decreased. It was concluded that PDGF-induced VSMC proliferation was related to the Nur77 expression and CREB phosphorylation. Atorvastatin reduced the Nur77 expression and, at the same time, inhibited the VSMC proliferation.
authors.affiliation: Department of Cardiology, Tongren Hospital, Wuhan University, Wuhan, 430060, China.
authors.forename: Liyue
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Tongren Hospital, Wuhan University, Wuhan, 430060, China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Dong
authors.affiliation: Department of Cardiology, Union Hospital, Tongji Medical University, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.affiliation: Department of Cardiology, Union Hospital, Tongji Medical University, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Qiutang
authors.initials: Q
authors.lastname: Zeng
authors.affiliation: Department of Cardiology, Union Hospital, Tongji Medical University, Huazhong University of Science and Technology, Wuhan, 430022, China. maoyi1007@gmail.com.
authors.forename: Yi
authors.initials: Y
authors.lastname: Mao
mesh_terms: D000818:Animals; D000069059:Atorvastatin; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism*; D006538:Heptanoic Acids / Q000494:pharmacology; D008297:Male; D032342:Muscle Cells / Q000166:cytology / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000378:metabolism; D057105:Nuclear Receptor Subfamily 4, Group A, Member 1 / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation; D010982:Platelet-Derived Growth Factor / Q000494:pharmacology*; D011758:Pyrroles / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C508137:Creb1 protein, rat; D017362:Cyclic AMP Response Element-Binding Protein; D006538:Heptanoic Acids; C539820:Nr4a1 protein, rat; D057105:Nuclear Receptor Subfamily 4, Group A, Member 1; D010982:Platelet-Derived Growth Factor; D011758:Pyrroles; D000069059:Atorvastatin