SOCS3 Stabilizes PARP1 to Suppress Adipogenic Transcription and Abdominal Adipogenesis in Avian.

Authors

Zheng Wang, Zixuan Tian, Liuying Qv, Mingyu Zhao, Qiangsen Zhao, Zhenhua Ma, Qiaoxian Yue, Zhongtao Yin, Zhuocheng Hou, Huifeng Li

Published in

FASEB journal : official publication of the Federation of American Societies for Experimental Biology. Volume 40. Issue 14. Pages e72136. Jul 31, 2026.

Abstract

Adipocyte differentiation is central to adipose tissue development, yet the regulatory mechanisms and transcriptional networks remain incompletely understood. Here, we demonstrate that suppressor of cytokine signaling 3 (SOCS3) plays a pivotal role in regulating avian adipogenesis by modulating adipogenic transcriptional programs. Multiplex immunofluorescence revealed that SOCS3 is enriched in PDGFRα⁺ preadipocytes within abdominal fat but declines during late differentiation. Functional studies in primary adipocytes and ICP1 cell line showed that SOCS3 knockdown promotes, whereas overexpression inhibits, adipogenic differentiation. Transcriptomic profiling indicated that SOCS3 depletion remodels the adipogenic transcriptional landscape, upregulating adipogenic and metabolic genes while downregulating transcriptional inhibitors. Mechanistically, proteomic analyses and co-immunoprecipitation identified poly(ADP-ribose) polymerase 1 (PARP1) as a SOCS3-binding partner. SOCS3 stabilizes PARP1 by suppressing its ubiquitination, leading to increased PAR levels and inhibition of adipogenesis. PARP1 interacts with PPARγ and represses its transcriptional activity through a mechanism independent of enzymatic PARylation. Importantly, ligand activation of PPARγ weakens its interaction with PARP1 and alleviates PARP1-mediated repression of its transcriptional activity. Collectively, these findings reveal a previously unrecognized SOCS3/PARP1 axis that modulates the transcriptional programs driving chicken adipocyte differentiation, underscoring its critical role in adipogenesis.

PMID:
42455636
Bibliographic data and abstract were imported from PubMed on 15 Jul 2026.

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