STIM2β is a Ca 2+ signaling modulator for the regulation of mitotic clonal expansion and PPARG2 transcription in adipogenesis.
Jeong SJ., Sim BW., Kim SU., Park CY.
Animal Study, published in FEBS J (2025) — 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
- FEBS J (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40344531
- PMCID
- PMC12326919
- DOI
- 10.1111/febs.70118
Abstract (original English)
Intracellular Ca 2+ is crucial in the regulation of adipocyte lipid metabolism and adipogenesis. In this study, we aimed to investigate the regulation mechanism of intracellular Ca 2+ levels ([Ca 2+ ] i ) during adipocyte differentiation. We found that the expression of stromal interaction molecule 2 beta (STIM2β), which is the inhibitor of store-operated Ca 2+ entry (SOCE), is upregulated throughout the differentiation process. Evaluation of [Ca 2+ ] i in 3 T3-L1 and primary stromal vascular fraction (SVF) cells revealed that the basal Ca 2+ level is downregulated after differentiation. Knockout (KO) of STIM2β in 3T3-L1 and primary SVF cells showed increased [Ca 2+ ] i , indicating the involvement of STIM2β in the regulation of [Ca 2+ ] i during adipogenesis. We further evaluated the function of STIM2β-mediated [Ca 2+ ] i in early and terminal differentiation of adipogenesis. Analysis of cell proliferation rate during mitotic clonal expansion (MCE) in wild-type and STIM2β KO 3T3-L1 cell lines revealed that a larger population of KO cells underwent G1 arrest, suggesting that reduced [Ca 2+ ] i by STIM2β induces MCE. Additionally, ablation of STIM2β increased differentiation efficiency, with more lipid accumulation and rapid transcriptional activation of adipogenic genes, especially proliferator-activator receptor γ2 (PPARG2). We found that PPARG2 transcription is regulated by s
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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