Col5a3 Likely Promotes Adipogenesis of 3T3-L1 Through Oxidative Phosphorylation

TL;DR

This study shows that Col5a3 affects fat cell development in 3T3-L1 cells, possibly through energy production processes.

Contribution

The study reveals a novel regulatory role of Col5a3 in adipogenesis via oxidative phosphorylation.

Findings

Col5a3 interference increased 3T3-L1 cell proliferation but reduced differentiation.

RNA-seq identified 368 differentially expressed genes, with oxidative phosphorylation being the most enriched pathway.

Col5a3 may regulate adipogenesis through oxidative phosphorylation in 3T3-L1 cells.

Abstract

Background: A recent study reported that a deficiency of Col5a3 reduces dermal fat. However, the regulatory mechanism of the Col5a3 gene on adipose deposition remains unclear. Methods: In this study, we assessed the effects of Col5a3 interference on the proliferation and differentiation of 3T3-L1 preadipocytes through CCK-8, EdU staining, cell cycle detection, RT-qPCR, Western blot, a triglyceride assay, and Oil Red O staining. RNA-seq was then performed on differentiated adipocytes to identify key differentially expressed genes (DEGs) and signaling pathways. Results: Col5a3 interference significantly promoted the proliferation of 3T3-L1 cells but inhibited their differentiation. RNA-seq analysis identified 368 DEGs, with the most significant enrichment observed in the oxidative phosphorylation pathway. Conclusions: This study demonstrates the regulatory role of Col5a3 in the proliferation and differentiation of preadipocytes, identifying various genes regulated by Col5a3 in adipogenesis. We speculate that Col5a3 may influence adipogenesis through the oxidative phosphorylation pathway in 3T3-L1 cells. The findings help gain a better understanding of the molecular mechanisms underlying fat deposition and obesity-related metabolic diseases.

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