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