title: Tetraspanin CD9 is involved in pancreatic damage during caerulein-induced acute pancreatitis in mice.
abstract: OBJECTIVE
  Pancreatic acinar cell necrosis and subsequent inflammatory response aggravate acute pancreatitis (AP). Tetraspanin CD9 has been reported to mediate inflammatory signaling by regulating molecular organization at the cell surface. This study aimed to investigate the role of CD9 in caerulein-induced AP (CIP) in mice.
  
  
  METHODS
  The expression of CD9 was detected in CIP in mice in vivo and cholecystokinin (CCK)/recombinant mouse tumor necrosis factor (rmTNF)-α induced pancreatic acinar cell death in vitro by quantitative real-time polymerase chain reaction, Western blot and immunofluorescence. The roles of CD9 in pancreatic acinar cell death and inflammatory response were further studied through the deletion of CD9 expression using small interfering RNA (siRNA).
  
  
  RESULTS
  CD9 was markedly upregulated in pancreatic tissues in mice during the early onset of CIP and was located mainly at the pancreatic acinar cell surface, which was associated with pancreatic damage. Additionally, incubation with CCK or rmTNF-α directly increased the expression of CD9 in isolated mice pancreatic acinar cells in vitro. The deletion of CD9 expression partially reversed both pancreatic acinar cell death induced by CCK and mRNA levels of proinflammatory cytokines produced by damaged acinar cells.
  
  
  CONCLUSIONS
  These results indicate that increased CD9 expression may be involved in pancreatic injury, possibly via the promotion of cytokine expressions in CIP in mice.
authors.affiliation: Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Xing
authors.forename: Jian Bo
authors.initials: JB
authors.lastname: Ni
authors.forename: Rong
authors.initials: R
authors.lastname: Wan
authors.forename: Mao Chun
authors.initials: MC
authors.lastname: Tang
authors.forename: Yan Ling
authors.initials: YL
authors.lastname: Hu
authors.forename: Ge
authors.initials: G
authors.lastname: Yu
authors.forename: Guo Jian
authors.initials: GJ
authors.lastname: Yin
authors.forename: Cong Ying
authors.initials: CY
authors.lastname: Chen
authors.forename: Yu Ting
authors.initials: YT
authors.lastname: Fan
authors.forename: Wen Qing
authors.initials: WQ
authors.lastname: Xiao
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Xing Peng
authors.initials: XP
authors.lastname: Wang
authors.forename: Guo Yong
authors.initials: GY
authors.lastname: Hu
mesh_terms: D061354:Acinar Cells / Q000276:immunology; D000208:Acute Disease; D000818:Animals; D002108:Ceruletide; D002766:Cholecystokinin / Q000235:genetics; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D015870:Gene Expression; D051379:Mice; D008807:Mice, Inbred BALB C; D010179:Pancreas / Q000503:physiopathology; D010195:Pancreatitis / Q000139:chemically induced / Q000235:genetics*; D012313:RNA / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D011897:Random Allocation; D015398:Signal Transduction / Q000235:genetics; D060245:Tetraspanin 29 / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D015854:Up-Regulation
chemical_list: C554870:Cd9 protein, mouse; D016207:Cytokines; D034741:RNA, Small Interfering; C039919:RNA, recombinant; D060245:Tetraspanin 29; D014409:Tumor Necrosis Factor-alpha; D012313:RNA; D002108:Ceruletide; D002766:Cholecystokinin
keywords: acinar cells; acute necrotizing pancreatitis; inflammation; mouse CD9 protein; pancreatitis