| Literature DB >> 25901193 |
Chenxi Wang1, Ting Wu2, Xiaojuan Hu2, Ritai Huang3, Feng Lian3, Weijun Wang3, Yuan Feng3, Bo Xie3, Zhenlei Hu3, Xinming Zhai3, Jidong Liu3, Jianmin Gu3, Yao Chen2, Jun Li1, Song Xue3.
Abstract
Thoracic aortic aneurysm (TAA) is progressive fatal aortic pathological dilation. However, the underlying molecular mechanisms are still largely unknown. Evidences suggest that endothelial cells and renin-angiotensin system may participate in the pathogenesis of TAA. This study aimed to investigate whether angiotensin II type 2 receptor (AT2) positive cells are involved in TAA formation. The mRNA level of AT2 is dramatically elevated in TAA compared with in controls. CD4(+)AT2(+) cells increased in both aortic wall and circulation of TAA patients. The levels of IL-1β and IL-17B in CD4(+)AT2(+) cells were lower than those in CD4(+)AT2(-) cells. When compared with endothelial cells (ECs) cultured alone, CD4(+)AT2(+) cells showed an inhibitory effect on proliferation and MMP2 expression in ECs, but CD4(+)AT2(-) cells promoted proliferation and MMP2 expression in ECs. Both CD4(+)AT2(+) and CD4(+)AT2(-) cells suppressed apoptosis of ECs. In conclusion, we have identified a novel population of CD4(+)AT2(+) T lymphocytes that show protective effect in TAA through inhibition of growth, apoptosis, and MMP2 expression in ECs.Entities:
Keywords: Angiotensin II type 2 receptor; endothelial cell; inflammation; matrix metalloprotease 2; thoracic aortic aneurysm
Year: 2015 PMID: 25901193 PMCID: PMC4399088
Source DB: PubMed Journal: Am J Transl Res Impact factor: 4.060