{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Batchu N"],"funding":["NIAID NIH HHS","NHLBI NIH HHS"],"pagination":["1638-1646"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5096552"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["36(8)"],"pubmed_abstract":["<h4>Objective</h4>Survival of immune and nonimmune cells relies on Axl, a receptor tyrosine kinase, which is implicated in hypertension. Activated T lymphocytes are involved in regulation of high blood pressure. The goal of the study was to investigate the role of Axl in T-lymphocyte functions and its contribution to salt-dependent hypertension.<h4>Approach and results</h4>We report increased apoptosis in peripheral blood from Axl(-/-) mice because of lower numbers of white blood cells mostly lymphocytes. In vitro studies showed modest reduction in interferon gamma production in Axl(-/-) type 1 T helper cells. Axl did not affect basic proliferation capacity or production of interleukin 4 in Axl(-/-) type 2 T helper cells. However, competitive repopulation of Axl(-/-) bone marrow or adoptive transfer of Axl(-/-) CD4(+) T cells to Rag1(-/-) mice showed robust effect of Axl on T lymphocyte expansion in vivo. Adoptive transfer of Axl(-/-) CD4(+) T cells was protective in a later phase of deoxycorticosterone-acetate and salt hypertension. Reduced numbers of CD4(+) T cells in circulation and in perivascular adventitia decreased vascular remodeling and increased vascular apoptosis in the late phase of hypertension.<h4>Conclusions</h4>These findings suggest that Axl is critical for survival of T lymphocytes, especially during vascular remodeling in hypertension."],"journal":["Arteriosclerosis, thrombosis, and vascular biology"],"pubmed_title":["Role of Axl in T-Lymphocyte Survival in Salt-Dependent Hypertension."],"pmcid":["PMC5096552"],"funding_grant_id":["P01 AI102851","R01 AI072690","R01 HL105623","R01 HL124018"],"pubmed_authors":["Wadosky KM","Morrell CN","Fowell DJ","Batchu N","Korshunov VA","Hughson A"],"additional_accession":[]},"is_claimable":false,"name":"Role of Axl in T-Lymphocyte Survival in Salt-Dependent Hypertension.","description":"<h4>Objective</h4>Survival of immune and nonimmune cells relies on Axl, a receptor tyrosine kinase, which is implicated in hypertension. Activated T lymphocytes are involved in regulation of high blood pressure. The goal of the study was to investigate the role of Axl in T-lymphocyte functions and its contribution to salt-dependent hypertension.<h4>Approach and results</h4>We report increased apoptosis in peripheral blood from Axl(-/-) mice because of lower numbers of white blood cells mostly lymphocytes. In vitro studies showed modest reduction in interferon gamma production in Axl(-/-) type 1 T helper cells. Axl did not affect basic proliferation capacity or production of interleukin 4 in Axl(-/-) type 2 T helper cells. However, competitive repopulation of Axl(-/-) bone marrow or adoptive transfer of Axl(-/-) CD4(+) T cells to Rag1(-/-) mice showed robust effect of Axl on T lymphocyte expansion in vivo. Adoptive transfer of Axl(-/-) CD4(+) T cells was protective in a later phase of deoxycorticosterone-acetate and salt hypertension. Reduced numbers of CD4(+) T cells in circulation and in perivascular adventitia decreased vascular remodeling and increased vascular apoptosis in the late phase of hypertension.<h4>Conclusions</h4>These findings suggest that Axl is critical for survival of T lymphocytes, especially during vascular remodeling in hypertension.","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Aug","modification":"2025-04-18T20:50:10.403Z","creation":"2019-03-27T02:28:17Z"},"accession":"S-EPMC5096552","cross_references":{"pubmed":["27365404"],"doi":["10.1161/ATVBAHA.116.307848","10.1161/atvbaha.116.307848"]}}