IL-1 stimulates ceramide accumulation without inducing apoptosis in intestinal epithelial cells
Background: In inflammatory bowel disease (IBD), cytokine levels (such as interleukin-1 (IL-1)) are elevated. We have shown previously that IL-1 activates phospholipid signaling pathways in intestinal epithelial cells (IEC), leading to increased ceramide levels. Aim: To determine whether ceramide in...
محفوظ في:
| المؤلف الرئيسي: | |
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| مؤلفون آخرون: | , , , |
| التنسيق: | article |
| منشور في: |
2002
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| الوصول للمادة أونلاين: | http://hdl.handle.net/10725/2820 http://dx.doi.org/10.1080/09629350210313 http://www.hindawi.com/journals/mi/2002/467015/abs/ |
| الوسوم: |
إضافة وسم
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| الملخص: | Background: In inflammatory bowel disease (IBD), cytokine levels (such as interleukin-1 (IL-1)) are elevated. We have shown previously that IL-1 activates phospholipid signaling pathways in intestinal epithelial cells (IEC), leading to increased ceramide levels. Aim: To determine whether ceramide induces apoptosis in IEC. Methods: Apoptosis was evaluated by annexin-Vbinding or Hoechst nuclear staining. Levels of bcl-2, bcl-x, bax, p53 and p21 were determined by Western blotting, and cell cycle analysis was determined by flow cytometry. Results: IL-1 increased ceramide accumulation in a time-dependent and concentration-dependent manner with a peak response at 4 h, with [IL-1] = 30 ng/ml. Neither IL-1 nor ceramide induced apoptosis in IEC, but they increased bcl-2 levels and decreased bax and p21 levels without affecting bcl-x and p53 levels. They also caused a slight but significant increase in the G2/M phase. These data suggest a role for ceramide in IBD and suggest a possible mechanism for the enhanced tumorigenic activity in IBD patients. |
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