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Tetraspanin CD 9 is involved in pancreatic damage during caerulein‐induced acute pancreatitis in mice
Author(s) -
Xing Miao,
Ni Jian Bo,
Wan Rong,
Tang Mao Chun,
Hu Yan Ling,
Yu Ge,
Yin Guo Jian,
Chen Cong Ying,
Fan Yu Ting,
Xiao Wen Qing,
Zhao Yan,
Wang Xing Peng,
Hu Guo Yong
Publication year - 2015
Publication title -
journal of digestive diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 51
eISSN - 1751-2980
pISSN - 1751-2972
DOI - 10.1111/1751-2980.12204
Subject(s) - acinar cell , cholecystokinin , proinflammatory cytokine , ceruletide , pancreatitis , tetraspanin , in vivo , downregulation and upregulation , medicine , cell , cancer research , endocrinology , inflammation , biology , receptor , genetics , microbiology and biotechnology , biochemistry , gene
Objective Pancreatic acinar cell necrosis and subsequent inflammatory response aggravate acute pancreatitis ( AP ). Tetraspanin CD 9 has been reported to mediate inflammatory signaling by regulating molecular organization at the cell surface. This study aimed to investigate the role of CD 9 in caerulein‐induced AP ( CIP ) in mice. Methods The expression of CD 9 was detected in CIP in mice in vivo and cholecystokinin ( CCK )/recombinant mouse tumor necrosis factor (rm TNF )‐α induced pancreatic acinar cell death in vitro by quantitative real‐time polymerase chain reaction, W estern blot and immunofluorescence. The roles of CD 9 in pancreatic acinar cell death and inflammatory response were further studied through the deletion of CD 9 expression using small interfering RNA (si RNA ). Results CD 9 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 rm TNF ‐α directly increased the expression of CD 9 in isolated mice pancreatic acinar cells in vitro . The deletion of CD 9 expression partially reversed both pancreatic acinar cell death induced by CCK and m RNA levels of proinflammatory cytokines produced by damaged acinar cells. Conclusion These results indicate that increased CD 9 expression may be involved in pancreatic injury, possibly via the promotion of cytokine expressions in CIP in mice.