title: Overexpression of Sterol Carrier Protein 2 in patients with hereditary cholesterol gallstones.
abstract: BACKGROUND
  Lithogenic bile is the major cause of cholesterol gallstone, but its pathogenesis is not well understood. The hypersecretion of biliary cholesterol is believed to be an important cause of lithogenic bile. Sterol Carrier Protein 2 (SCP2) participates in cholesterol trafficking and lipid metabolism in hepatocytes and may play a key role in cholesterol gallstone formation.
  
  
  METHODS
  21 cholesterol gallstone genealogies were studied to investigate the expression of SCP2 gene in liver tissue of hereditary and non-hereditary cholesterol gallstone patients as well as non-gallstone patients. The mRNA expression of liver SCP2 in 28 hereditary patients, 30 non-hereditary cholesterol gallstone patients and 32 non-gallstone patients was measured by Reverse Transcription Polymerase Chain Reaction (RT-PCR). The protein expression of liver SCP2 was also detected in all the patients by Western blotting. At the same time, the bile was also analyzed with biochemical techniques and the Cholesterol Saturation Index (CSI) was calculated.
  
  
  RESULTS
  The mRNA and protein expression of SCP2 was significantly increased in cholesterol gallstone patients compared to those of non-gallstone patients. Moreover, SCP2 was expressed at higher levels in hereditary cholesterol gallstone patients than that of non-hereditary cholesterol gallstone patients. There was significant difference observed in CSI between cholesterol gallstone patients and non-gallstone patients, but not in CSI between hereditary and non-hereditary cholesterol gallstone patients.
  
  
  CONCLUSIONS
  SCP2 was overexpressed in hereditary cholesterol gallstone patients compared to non-hereditary cholesterol gallstone patients. This finding indicated that SCP2 might be one of the genetic factors contributing to cholesterol gallstone formation, which was always accompanied by the increase of bile lithogenicity.
authors.affiliation: Department of Surgery, Tianjin Nankai Hospital, Nankai Clinical School of Medicine, Tianjin Medical University, 122 Sanwei Road Nankai District, Tianjin 300100, PR China.
authors.forename: YunFeng
authors.initials: Y
authors.lastname: Cui
authors.forename: ZhongLian
authors.initials: Z
authors.lastname: Li
authors.forename: ErPeng
authors.initials: E
authors.lastname: Zhao
authors.forename: YanFeng
authors.initials: Y
authors.lastname: Jia
authors.forename: DongHua
authors.initials: D
authors.lastname: Li
authors.forename: Ju
authors.initials: J
authors.lastname: Zhang
authors.forename: NaiQiang
authors.initials: N
authors.lastname: Cui
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D001646:Bile / Q000737:chemistry; D002352:Carrier Proteins / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D002769:Cholelithiasis / Q000235:genetics / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D055815:Young Adult
chemical_list: D002352:Carrier Proteins; D012333:RNA, Messenger; C072087:sterol carrier proteins; D002784:Cholesterol