Effect of Has3 deficiency on gene expression in the aorta of a mouse model of abdominal aortic aneurysms

HAS3-derived hyaluronan (HA) is implicated in inflammatory processes of multiple human diseases. Employing a model of Angiotensin II -induced abdominal aortic aneuryms (AAA), we here examine the gene expression profiles of the aorta from Has3-deficient (Apoe/Has3-DKO) and Has3-competent (Apoe-KO) mice. We find a set of 53 differentially regulated genes involved in inflammation and leukocyte cell migration. Specifically, CXCL3 was profoundly upregulated in the aorta of Apoe/Has3-DKO, together with the pathways 'Agranulocyte adhesion and diapedesis' and 'Granulocyte adhesion and diapedesis`. Our data highlight the role of HAS3 as regulator of inflammation and immune cell recruitment in the devlopment of AAA. Overall design: RNA seq profiling of aortic tissue from Apoe/Has3-DKO Apoe-KO mice 3 days post Angiotensin II treatment.