Perivascular Adipocytes' Adipogenesis Is Defined by Their Anatomical Location in the Descending Thoracic Aorta.

Cardiovascular diseases such as hypertension alter thoracic aorta structure. The role that the outer layer of the aorta, its perivascular adipose tissue (PVAT), plays in the pathogenesis of these alterations is poorly understood. In the descending thoracic aorta, PVAT is organized into three distinct strips: one located anterior to the aorta (AP) and two positioned laterally (LP). Genetic tracing indicates differences in the ontogeny of LP and AP, but the implications of these developmental differences and PVAT distribution on adipocyte development remain unknown. We hypothesize that the anatomical location of adipocyte progenitors influences their adipogenic potential and vasoactive functions. PVAT from LP and AP was collected from male SD rats at 10 wks of age (n = 7) to harvest adipocyte progenitors that were differentiated to adipocytes in adipogenic media. Adipogenesis was evaluated after induction and we performed next-generation RNA-seq on progenitors and adipocytes. We then employed Gene Set Enrichment Analysis for enrichment and network analyses. LP progenitors exhibited a 1.13-fold higher adipogenesis rate compared to those from AP. DEG analysis revealed LP had higher expression of adipogenic regulators and basal collagens Col4a2 and Col4a4. When challenged with angiotensin-II, adipocyte progenitors from LP maintained their adipogenic capacity and adipocytes from the same site maintained their secretion of adiponectin at higher rates than AP cells. However, treatment with a Piezo1 mechanoreceptor agonist reduced LP's adipogenic capacity and diminished their adiponectin secretion. These findings highlight site-specific differences in adipogenic activity, extracellular matrix composition, and the secretion of the vasoactive adipokine adiponectin between the LP and AP PVAT strips of the thoracic aorta, suggesting potential functional distinctions in vascular health and disease.