Upregulation of cIAP2 in regenerating colonocytes in ulcerative colitis
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Upregulation of cIAP2 in regenerating colonocytes in ulcerative colitis. / Seidelin, J.B.; Vainer, Ben; Andresen, L.; Nielsen, Ole Haagen.
In: Virchows Archiv, Vol. 451, No. 6, 2007, p. 1031-1038.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Upregulation of cIAP2 in regenerating colonocytes in ulcerative colitis
AU - Seidelin, J.B.
AU - Vainer, Ben
AU - Andresen, L.
AU - Nielsen, Ole Haagen
PY - 2007
Y1 - 2007
N2 - It has been reported that colonocytes in ulcerative colitis (UC) upregulate anti-apoptotic cytoprotective pathways. An expression-profiling study of apoptosis-related genes suggested that the cellular inhibitor of apoptosis protein-2 (cIAP2) could be upregulated in epithelial cells in UC. The role of cIAP2 in active UC was therefore investigated. Fourteen patients with active UC and 12 control subjects who underwent routine colonoscopy for control of their disease or as part of their examination program for irritable bowel syndrome were included. cIAP1 and cIAP2 expression was investigated by polymerase chain reaction, Western blotting, and immunohistochemistry. The regulation and role of cIAP2 for apoptosis was further investigated in cell cultures. cIAP2, but not cIAP1, was upregulated during active UC in regenerative epithelial cells. A similar upregulation was found in cell lines stimulated with proinflammatory cytokines and was dependent on nuclear factor kappaB activation. Inhibition of cIAP2 increases the susceptibility of epithelial cells to Fas ligation. Inflammation during active UC thus causes an upregulation of cIAP2 in regenerating epithelium, which renders the cells less susceptible to Fas ligation. This might play a role in regeneration of the epithelium but might additionally be implicated in carcinogenesis of UC.
AB - It has been reported that colonocytes in ulcerative colitis (UC) upregulate anti-apoptotic cytoprotective pathways. An expression-profiling study of apoptosis-related genes suggested that the cellular inhibitor of apoptosis protein-2 (cIAP2) could be upregulated in epithelial cells in UC. The role of cIAP2 in active UC was therefore investigated. Fourteen patients with active UC and 12 control subjects who underwent routine colonoscopy for control of their disease or as part of their examination program for irritable bowel syndrome were included. cIAP1 and cIAP2 expression was investigated by polymerase chain reaction, Western blotting, and immunohistochemistry. The regulation and role of cIAP2 for apoptosis was further investigated in cell cultures. cIAP2, but not cIAP1, was upregulated during active UC in regenerative epithelial cells. A similar upregulation was found in cell lines stimulated with proinflammatory cytokines and was dependent on nuclear factor kappaB activation. Inhibition of cIAP2 increases the susceptibility of epithelial cells to Fas ligation. Inflammation during active UC thus causes an upregulation of cIAP2 in regenerating epithelium, which renders the cells less susceptible to Fas ligation. This might play a role in regeneration of the epithelium but might additionally be implicated in carcinogenesis of UC.
U2 - 10.1007/s00428-007-0517-1
DO - 10.1007/s00428-007-0517-1
M3 - Journal article
C2 - 17972100
VL - 451
SP - 1031
EP - 1038
JO - Virchows Archiv
JF - Virchows Archiv
SN - 0945-6317
IS - 6
ER -
ID: 4042133