Abstract P309: Descending Thoracic Aorta Perivascular Adipocytes Adipogenesis Is Defined By Their Anatomical Location

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Hypertension, atherosclerosis, and aneurysms alter thoracic aorta structure. Aortic lesions in these diseases show unique anatomical distribution. Calcifications and atherosclerotic lesions occur more frequently in the posterior wall of the aorta compared to other regions. Descending thoracic aorta's perivascular adipose tissue (PVAT) is distributed in 3 strips: one is located anterior to the aorta ( AP ), and two positioned laterally to the posterior wall of the vessel and adjacent to thoracic vertebrae ( LP ). Evidence indicates PVAT LP’s adipocytes derive from different progenitors than those from AP. The implications of this ontology and aortic PVAT distribution on the development of its adipocytes and other cellular components is unknown. We hypothesize that progenitor’s anatomical location influences their adipogenic potential. LP and AP were collected from male SD rats (n=7) at 10 wks of age to harvest progenitors by outgrowth expansion. Progenitors were differentiated for 4 d in adipogenic media. Adipogenesis was evaluated by lipid droplet and triglyceride quantification using Live-Cell ® imaging. RNA from progenitors and adipocytes was sequenced in Illumina NextSeqData, and Differential Expressed Genes identified. Enrichment and network analyses were performed in Ingenuity Pathways (IPA). Ontogeny gene markers Myf5 and Sm22a had higher expression in LP than AP. LP progenitors had 213% higher adipogenesis rate than AP (P<0.05). This change was accompanied by increased transcription of adipogenesis regulator Cepba and the intracellular FA transporter Fabp4 and lower expression of the lipase ATGL ( Pnpla2 ) and the membrane channel supporting FA export FATP6 ( Slc27a6 ) in LP vs. AP. IPA analysis showed upregulation of antiadipogenic pathways adrenomedullin and endothelin in AP. Anatomical site influenced the extracellular marker gene profile with LP having a higher transcription of collagens 1a1, 6a1, and elastin vs. AP. Taken together, our findings provide evidence supporting differences in adipogenic activity and extracellular matrix secretion between aorta’s LP and AP PVAT. These differences may support anatomical location as a predisposing factor for aortic lesions associated with hypertension, atherosclerosis, and aneurysms.