title: Visfatin stimulates a cellular renin-angiotensin system in cultured rat mesangial cells.
abstract: OBJECTIVE
  Visfatin is a newly identified proinflammatory adipocytokine whose plasma levels have been reported to be higher in subjects with type 2 diabetes mellitus. Recent studies have shown that visfatin increases the synthesis of profibrotic molecules in mesangial cells (MCs) and thus plays an important role in the pathogenesis of diabetic nephropathy. However, the mechanism by which visfatin induces kidney injury is unknown. The renin-angiotensin system (RAS) plays pivotal roles in renal diseases. Therefore, in this study the effect of visfatin on the regulation of RAS in MCs was examined.
  
  
  METHODS
  Cultured rat MCs were treated with different doses of visfatin. We used real-time polymerase chain reaction to detect mRNA expression of renin, angiotensinogen (AGT), angiotensin-converting enzyme (ACE), angiotensin II (Ang II) type 1 receptor (AT1), and Ang II type 2 receptor (AT2); western blot analysis for expression of ANG and AT1; and radioimmunoassay to measure Ang II production from MCs in the supernatants of culture media.
  
  
  RESULTS
  Visfatin treatments increased renin, angiotensinogen (AGT), AT1 mRNA, and AGT, AT1 protein expression, as well as Ang II levels in a dose-dependent manner but did not affect ACE and AT2 mRNA levels in cultured rat MCs.
  
  
  CONCLUSIONS
  Our findings suggest that visfatin imparts a detrimental effect on diabetic nephropathy at least partly through the activation of intrarenal RAS.
authors.affiliation: Department of Endocrinology, The Second Affiliated Hospital, Sun Yat-Sen University, Guangzhou, PR, China.
authors.forename: Qiong
authors.initials: Q
authors.lastname: Huang
authors.forename: Ying
authors.initials: Y
authors.lastname: Guo
authors.forename: Hua
authors.initials: H
authors.lastname: Zeng
authors.forename: Wenfeng
authors.initials: W
authors.lastname: Xie
authors.forename: Haiyan
authors.initials: H
authors.lastname: Yan
authors.forename: Helin
authors.initials: H
authors.lastname: Ding
mesh_terms: D000803:Angiotensin I / Q000096:biosynthesis; D000804:Angiotensin II / Q000096:biosynthesis; D000808:Angiotensinogen / Q000096:biosynthesis; D000818:Animals; D002460:Cell Line; D003928:Diabetic Nephropathies / Q000209:etiology; D005920:Glomerular Mesangium / Q000166:cytology / Q000378:metabolism*; D054409:Nicotinamide Phosphoribosyltransferase / Q000494:pharmacology*; D007703:Peptidyl-Dipeptidase A / Q000096:biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D044140:Receptor, Angiotensin, Type 1 / Q000096:biosynthesis; D011945:Receptors, Angiotensin / Q000096:biosynthesis; D012083:Renin / Q000096:biosynthesis; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology
chemical_list: D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D000804:Angiotensin II; D000803:Angiotensin I; D054409:Nicotinamide Phosphoribosyltransferase; D007703:Peptidyl-Dipeptidase A; D012083:Renin