{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(2)"],"submitter":["Wang C"],"journal":["American journal of translational research"],"pagination":["232-41"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4399088"],"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-1? 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."],"repository":["biostudies-other"],"pmcid":["PMC4399088"],"data_source":["Europe PMC"],"pubmed_authors":["Liu J","Li J","Hu Z","Wang C","Hu X","Feng Y","Huang R","Lian F","Zhai X","Xue S","Wang W","Gu J","Chen Y","Wu T","Xie B"],"additional_accession":[]},"is_claimable":false,"name":"Identification and characterization of CD4(+)AT2(+) T lymphocyte population in human thoracic aortic aneurysm.","description":"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-1? 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.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 ","modification":"2019-03-27T01:50:00Z","creation":"2019-03-27T01:50:00Z"},"accession":"S-EPMC4399088","cross_references":{"pubmed":["25901193"]}}