PRDM16 Enhances Osteoblastogenic RUNX2 via Canonical WNT10b/β-CATENIN Pathway in Testosterone-Treated Hypogonadal Men

PRDM16 Enhances Osteoblastogenic RUNX2 via Canonical WNT10b/β-CATENIN Pathway in Testosterone-Treated Hypogonadal Men

We previously reported that <i>PRDM16</i> mediated the improvement in body composition in testosterone (T)-treated hypogonadal men by shifting adipogenesis to myogenesis. Previous preclinical studies suggest that <i>Prdm16</i> regulates <i>Runx2</i>, an important...

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Bibliographic Details
Main Authors: Siresha Bathina, Mia Prado, Virginia Fuenmayor Lopez, Georgia Colleluori, Lina Aguirre, Rui Chen, Dennis T. Villareal, Reina Armamento-Villareal
Format: Article
Language:English
Published: MDPI AG 2025-01-01
Series:Biomolecules
Subjects:
PRDM16
RUNX2
osteoblastogenesis
BMD
Online Access:https://www.mdpi.com/2218-273X/15/1/79
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Summary:We previously reported that <i>PRDM16</i> mediated the improvement in body composition in testosterone (T)-treated hypogonadal men by shifting adipogenesis to myogenesis. Previous preclinical studies suggest that <i>Prdm16</i> regulates <i>Runx2</i>, an important osteoblastic transcription factor, expression and activity. However, the changes in <i>PRDM16</i>, and other genes/proteins involved in osteoblastogenesis with T therapy in hypogonadal men are unexplored. We investigated the role of PRDM16 in RUNX2 activation by measuring changes in gene expression in peripheral blood monocytes (PBMCs) and proteins in the serum of hypogonadal men after T therapy for 6 months. Likewise, we evaluated changes in the WNT10b—β-CATENIN signaling pathway by gene expression and protein analyses. We found significant increases in <i>PRDM16</i> and <i>RUNX2</i> expression in PBMCs together with significant increases in serum proteins at 6 months when compared to baseline. There were also increases in gene and protein expressions of WNT10b, and β-CATENIN at 6 months. Furthermore, we found a significant positive correlation between % changes in PRDM16 and WNT10b. Our results suggest that T therapy activates PRDM16, leading to enhanced signaling in the canonical WNT10b—β-CATENIN-RUNX2 pathway, the pathway involved in osteoblastogenesis. The above findings may account for the improvement in bone density and quality in hypogonadal men treated with T.
ISSN:2218-273X

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