Posters

Adipocyte/progenitor communication axis controls beige adipogenesis.

Presenting Author Academic/Professional Position

Briana Noel Cortez

Academic Level (Author 1)

Medical Student

Discipline Track

Biomedical Science

Abstract Type

Research/Clinical

Abstract

The unique capacity of inguinal white adipose tissue (iWAT) to brown has emerged as a promising therapeutic approach for treating obesity and its adverse complications. Both white and beige adipose arise from a subpopulation of perivascular adipocyte progenitor cells (APC) expressing SM22 (Smooth Muscle Protein 22-Alpha). However, the early signaling events controlling ACP differentiation to beige adipocytes are still unknown.

To uncover the stromal cells heterogeneity during beige adipogenesis, we performed a single cell RNA-sequencing of iWAT under control condition, treatment with β3-adrenergic receptor (ADRB3) agonist or exposure to cold. ScRNA-seq revealed the landscape of APCs undergoing beige adipogenesis. We identified a distinct subpopulation of APCs that accumulate in response to the stimulations but only cold induced their differentiation to beige adipocytes. Further investigation using RNA-seq of sorted APCs and lineage tracing mice models demonstrate that under cold challenge, beige adipocyte recruitment is a multi-step signaling process involving paracrine communication between mature adipocytes and vascular progenitors. This process involves: (1) ADRB3 activation of adipocytes, followed by (2) lipids release by mature adipocytes (3) that induce a metabolic switch and ADRB1 expression in SM22+ APCs. Activation of ADRB1 by catecholamine released under cold exposure promotes primed APCs differentiation to beige adipocytes.

Altogether, our data reveal existence of a necessary adipocyte/APC communication axis for beige adipogenesis.

Presentation Type

Poster

This document is currently not available here.

Share

COinS
 

Adipocyte/progenitor communication axis controls beige adipogenesis.

The unique capacity of inguinal white adipose tissue (iWAT) to brown has emerged as a promising therapeutic approach for treating obesity and its adverse complications. Both white and beige adipose arise from a subpopulation of perivascular adipocyte progenitor cells (APC) expressing SM22 (Smooth Muscle Protein 22-Alpha). However, the early signaling events controlling ACP differentiation to beige adipocytes are still unknown.

To uncover the stromal cells heterogeneity during beige adipogenesis, we performed a single cell RNA-sequencing of iWAT under control condition, treatment with β3-adrenergic receptor (ADRB3) agonist or exposure to cold. ScRNA-seq revealed the landscape of APCs undergoing beige adipogenesis. We identified a distinct subpopulation of APCs that accumulate in response to the stimulations but only cold induced their differentiation to beige adipocytes. Further investigation using RNA-seq of sorted APCs and lineage tracing mice models demonstrate that under cold challenge, beige adipocyte recruitment is a multi-step signaling process involving paracrine communication between mature adipocytes and vascular progenitors. This process involves: (1) ADRB3 activation of adipocytes, followed by (2) lipids release by mature adipocytes (3) that induce a metabolic switch and ADRB1 expression in SM22+ APCs. Activation of ADRB1 by catecholamine released under cold exposure promotes primed APCs differentiation to beige adipocytes.

Altogether, our data reveal existence of a necessary adipocyte/APC communication axis for beige adipogenesis.