کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1931222 | 1050546 | 2010 | 6 صفحه PDF | دانلود رایگان |

CD26/DPP-4 is abundantly expressed on capillary of inflamed lesion as well as effector T cells. Recently, CD26/dipeptidyl peptidase 4 (DPP-4) inhibition has been used as a novel oral therapeutic approach for patients with type 2 diabetes. While accumulating data indicate that vascular inflammation is a key feature of both micro- and macro-vascular complications in diabetes, the direct role of CD26/DPP-4 in endothelial biology is to be elucidated. We herein showed that proinflammatory cytokines such as tumor necrosis factor or interleukin-1 reduce expression of CD26 on microvascular endothelial cells, and that genetical or pharmacological inhibition of CD26/DPP-4 enhances endothelial growth both in vitro and in vivo. With DPP-4 inhibitors being used widely in the treatment of type 2 diabetes, our data strongly suggest that DPP-4 inhibition plays a pivotal role in endothelial growth and may have a potential role in the recovery of local circulation following diabetic vascular complications.
Research highlights
► TNF-α or IL-1β induces EC proliferation with reduction of CD26 expression.
► CD26 siRNA or DPP-4 inhibition enhances TNF-α or IL-1β-induced EC proliferation.
► Loss of CD26/DPP-4 enhances aortic sprouting induced by TNF-α or IL-1β.
► Capillary formation induced by TNF-α or IL-1β is enahced in the CD26−/− mice.
Journal: Biochemical and Biophysical Research Communications - Volume 401, Issue 1, 8 October 2010, Pages 7–12