SOCS2 Negatively Regulates Proliferation and Adipogenic Differentiation of Porcine Adipose-Derived Mesenchymal Stem Cells.
Shi H., Chen L., Gao J., Wang F., Liu Y.
Animal Study, published in Anim Genet (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Anim Genet (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42297742
- DOI
- 10.1002/age.70142
Abstract (original English)
Suppressor of cytokine signaling 2 (SOCS2) is a classical feedback inhibitor of JAK-STAT signaling, but its role in porcine adipose-derived mesenchymal stem cells (PADSCs) and fat deposition remains unclear. Here, we investigated the function and mechanism of SOCS2 in PADSC proliferation and adipogenic differentiation. SOCS2 overexpression reduced colony number, slowed CCK-8 growth curves, and induced G0/G1 arrest, whereas SOCS2 knockdown enhanced proliferation and promoted the G1/S transition. In parallel, SOCS2 overexpression decreased lipid droplet accumulation and downregulated adipogenic markers, while SOCS2 silencing produced the opposite effects, indicating that SOCS2 negatively regulates both PADSC expansion and adipocyte formation. Transcriptomic analysis showed that SOCS2 mainly influenced pathways related to extracellular matrix organization, cell cycle, and cytokine/inflammatory signaling. At the protein level, SOCS2 silencing increased total JAK2 and STAT3, whereas SOCS2 overexpression reduced JAK2 abundance and STAT3 activation, accompanied by concordant changes in Cyclin D1, CDK2, and PCNA. Collectively, these results suggest that SOCS2 exerts dual negative effects on PADSC proliferation and adipogenic differentiation, accompanied by changes in JAK2-STAT3 signaling. These findings provide functional evidence supporting SOCS2 as a candidate gene related to porcine
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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