title: Ghrelin improves vascular autophagy in rats with vascular calcification.
abstract: BACKGROUND
  This study aimed to investigate whether ghrelin ameliorated vascular calcification (VC) through improving autophagy.
  
  
  METHODS
  VC model was induced by nicotine plus vitamin D3in rats and β-glycerophosphate in vascular smooth muscle cell (VSMC). Calcium deposition was detected by von Kossa staining or alizarin red S staining. ALP activity was also detected. Western blot was used to assess the protein expression.
  
  
  RESULTS
  Ghrelin treatment attenuated the elevation of calcium deposition and ALP activity in VC model both in vivo and in vitro. Interesting, the protein levels of autophagy markers, LC3 and beclin1 were significantly upregulated by ghrelin in VC model. An autophagy inhibitor, 3-methyladenine blocks the ameliorative effect of ghrelin on VC. Furthermore, protein expressions of phosphate-AMPK were increased by ghrelin treatment both in calcified aorta and VSMC. The effect of ghrelin on autophagy induction and VC attenuation was prevented by AMPK inhibitor, compound C.
  
  
  CONCLUSIONS
  Our results suggested that ghrelin improved autophagy through AMPK activation, which was resulted in VC amelioration. These data maybe throw light on prevention and therapy of VC.
authors.affiliation: Department of Geriatric Medicine, Affiliated Nanshan Hospital of Guangdong Medical University, China. Electronic address: dr_xumm@sina.com.
authors.forename: Mingming
authors.initials: M
authors.lastname: Xu
authors.affiliation: Department of Geriatric Medicine, Affiliated Nanshan Hospital of Guangdong Medical University, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Geriatric Medicine, Affiliated Nanshan Hospital of Guangdong Medical University, China.
authors.forename: Chenfang
authors.initials: C
authors.lastname: Song
authors.affiliation: Department of Geriatric Medicine, Affiliated Nanshan Hospital of Guangdong Medical University, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Chen
authors.affiliation: Department of Endocrine, Affiliated Nanshan Hospital of Guangdong Medical University, China.
authors.forename: Shuyan
authors.initials: S
authors.lastname: Gui
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000473:pathology; D001343:Autophagy / Q000187:drug effects*; D002118:Calcium / Q000378:metabolism; D002762:Cholecalciferol; D004195:Disease Models, Animal; D054439:Ghrelin / Q000494:pharmacology*; D005994:Glycerophosphates; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D009538:Nicotine; D051381:Rats; D017207:Rats, Sprague-Dawley; D061205:Vascular Calcification / Q000188:drug therapy* / Q000473:pathology
chemical_list: D054439:Ghrelin; D005994:Glycerophosphates; D002762:Cholecalciferol; D009538:Nicotine; D055372:AMP-Activated Protein Kinases; D002118:Calcium; C031463:beta-glycerophosphoric acid
keywords: 3-methyladenine; AMPK; Autophagy; Compound C; Ghrelin; Vascular calcification