“…Transcripts more highly detected in the aortic root of LDS mice relative to the ascending aorta included Agtr1a, which codes for angiotensin II receptor type 1a, a known contributor to LDS pathogenesis, and Gata4, which codes for a transcription factor known to positively regulate Agtr1a expression in the heart 44,45 . CCAAT enhancer binding protein beta (Cebpb), a pro-inflammatory mediator 46 , and maternally expressed gene 3 (Meg3), a long non-coding RNA (lncRNA) that negatively regulates TGF-β signaling and promotes VSMC proliferation [47][48][49][50] , were also enriched in this region. In contrast, expression of cardiac mesoderm enhancer-associated noncoding RNA (Carmn), a positive regulator of VSMC contractile function that is downregulated in vascular disease, and expression of Myh11, a marker of differentiated VSMCs, was enriched in the distal ascending aorta, a region that is only mildly affected in LDS mouse models 49,[51][52][53] .…”