title: Impaired regulator of G protein signaling 2 transcription facilitates vascular remodeling in injured rat aorta.
abstract: BACKGROUND
  The activation of Gq-protein-coupled receptors induces proliferation of vascular smooth muscle cells (VSMCs) proliferation and is involved in vascular remodeling. The regulator of G protein signaling 2 (RGS2), which accelerates the termination of Gq protein signaling, may play a role in vascular remodeling. However, this role remains unclear.
  
  
  METHODS
  Aortic balloon injury or sham operation was produced in male Wistar rats. Histological examination and gene expression analysis were performed after surgery. In cultured VSMCs after modulation of RGS2 expression, cell proliferation was also evaluated.
  
  
  RESULTS
  At day 3 after injury, RGS2 transcription was reduced by 52.8% (P <0.05 vs. sham group) with vascular remodeling. In cultured VSMCs stimulated by endothelin-1, phenylephrine or angiotensin II, the proliferation of RGS2 overexpressed cells was significantly inhibited; the proliferation of RGS2 downregulated cells was significantly promoted, compared with that of RGS2 normal cells. Moreover, after incubation with angiotensin II of high concentration (>10 μmol/l) or long term (>8 h), the RGS2 expression was clearly downregulated in cultured VSMCs. Administration of an angiotensin receptor blocker, valsartan (20 mg/kg per day) starting from 1 week preballoon injury to 3 days after injury, restored aortic RGS2 transcription and improved vascular remodeling.
  
  
  CONCLUSIONS
  These results suggested that the inhibiting effect of RGS2 on VSMC proliferation is downregulated in vascular remodeling of injured rat aorta, and this effect is likely to be mediated by angiotensin II signaling.
authors.affiliation: aDepartment of Cardiology, Peking University First Hospital, Beijing, China bDepartment of Biochemistry, National Cerebral and Cardiovascular Center, Osaka, Japan cCardiology Division, Cardiovascular Research Center, Rhode Island Hospital and Alpert Medical School of Brown University, Providence, Rhode Island, USA dDepartment of Endocrinology, Beijing Aerospace Center Hospital eDepartment of Physiology, School of Basic Medical Sciences, Peking University, Beijing, China.
authors.forename: Yuanjie
authors.initials: Y
authors.lastname: Mao
authors.forename: Jialin
authors.initials: J
authors.lastname: Su
authors.forename: Lei
authors.initials: L
authors.lastname: Lei
authors.forename: Lei
authors.initials: L
authors.lastname: Meng
authors.forename: Yongfen
authors.initials: Y
authors.lastname: Qi
authors.forename: Yong
authors.initials: Y
authors.lastname: Huo
authors.forename: Chaoshu
authors.initials: C
authors.lastname: Tang
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000293:injuries / Q000378:metabolism / Q000473:pathology*; D049109:Cell Proliferation; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics*; D012313:RNA / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D043562:Receptors, G-Protein-Coupled / Q000096:biosynthesis / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D013777:Tetrazoles / Q000494:pharmacology; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology; D000068756:Valsartan; D066253:Vascular Remodeling / Q000187:drug effects / Q000235:genetics*; D057772:Vascular System Injuries / Q000235:genetics* / Q000378:metabolism / Q000473:pathology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D013777:Tetrazoles; D012313:RNA; D000068756:Valsartan; D014633:Valine