title: Association of all-trans retinoic acid treatment with the renin-angiotensin aldosterone system expression in glomerulosclerosis rats.
abstract: OBJECTIVE
  All-trans retinoic acid (ATRA), a promising therapeutic agent, has been confirmed in animal experiments as playing a protective role against renal diseases. The renin-angiotensin aldosterone system (RAAS) plays a key role in the pathogenesis of renal diseases, and RAAS inhibitors can prevent the progression of kidney diseases. In our previous study, we found that ATRA could play a protective role against glomerulosclerosis (GS) lesions in rats, and its effect was similar to RAAS inhibitors. However, whether ATRA treatment was associated with RAAS expression was not clear.
  
  
  METHODS
  Six-week-old male Wistar rats were divided into three groups: sham operation group (SHO), glomerulosclerosis model group without treatment (GS) and GS model group treated with ATRA (GA). At the end of 13 weeks, the relevant samples were collected and analyzed.
  
  
  RESULTS
  The mRNA and protein expression of angiotensin-converting enzyme 1 (ACE1) in the GS group was notably higher when compared with the SHO group. However, mRNA and protein expression of ACE1 in the ATRA treatment group was markedly down-regulated when compared with the GS group. Angiotensin-converting enzyme 2 (ACE2) expression (mRNA or protein) in the GS group was reduced compared with that in the SHO group, and ATRA markedly increased the mRNA and protein expression of ACE2 compared with the GS group. The levels of protein expression of angiotensin I and angiotensin II were significantly up-regulated in the GS group compared with those in the SHO group, and ATRA reduced their expression in the GA group when compared with the GS group.
  
  
  CONCLUSIONS
  ATRA is associated with RAAS expression in GS rats, but its detailed mechanism needs to be elucidated by further research.
authors.affiliation: 1Department of Pediatric Nephrology, The First Affiliated Hospital of GuangXi Medical University, Nanning, Guangxi, China.
authors.forename: Tian-Biao
authors.initials: TB
authors.lastname: Zhou
authors.forename: Wei-Feng
authors.initials: WF
authors.lastname: Wu
authors.forename: Yuan-Han
authors.initials: YH
authors.lastname: Qin
authors.forename: Sheng-Sheng
authors.initials: SS
authors.lastname: Yin
mesh_terms: D000803:Angiotensin I / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism; D000085962:Angiotensin-Converting Enzyme 2; D000818:Animals; D024141:Collagen Type IV / Q000378:metabolism; D005353:Fibronectins / Q000378:metabolism; D005921:Glomerulonephritis / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D007678:Kidney Glomerulus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System / Q000187:drug effects*; D014212:Tretinoin / Q000494:pharmacology*
chemical_list: D024141:Collagen Type IV; D005353:Fibronectins; D012333:RNA, Messenger; D000804:Angiotensin II; D014212:Tretinoin; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; C000705329:Ace2 protein, rat; D000085962:Angiotensin-Converting Enzyme 2
keywords: All-trans retinoic acid; angiotensin I; angiotensin II; angiotensin-converting enzyme 1; angiotensin-converting enzyme 2; glomerulosclerosis; renin–angiotensin aldosterone system