1110025M09Rik-encoded protein regulates adipogenic differentiation in murine bone marrow stromal cells.
Wang X., Du S., Xing S., Zhu E., Zhou J., Wang B.
Animal Study, published in Cell Signal (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
- Cell Signal (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40744330
- DOI
- 10.1016/j.cellsig.2025.112030
Abstract (original English)
Bone marrow adipose tissue (BMAT) plays a pivotal role in skeletal health and metabolism, yet the molecular mechanisms governing the commitment of bone marrow stromal cells (BMSCs) to the adipocyte lineage remain incompletely understood. Here, we identified 1110025M09Rik, a locus previously annotated as a long non-coding RNA (LncRNA), which contains an open reading frame (ORF) encoding a functional protein essential for adipogenesis. Overexpression of 1110025M09Rik significantly enhanced adipogenic differentiation in both ST2 stromal cells and primary BMSCs. Conversely, the knockdown of 1110025M09Rik resulted in reduced lipid accumulation and decreased expression of adipocyte markers in these cells. In vivo, deletion of 1110025M09Rik led to decreased bone marrow fat deposition in middle-aged mice and impaired adipogenic capacity of BMSCs isolated from knockout mice. Mechanistically, loss of 1110025M09Rik resulted in upregulation of kininogen 2 (Kng2), which we identified as a negative regulator of adipocyte differentiation. Importantly, silencing Kng2 restored the adipogenic potential in 1110025M09Rik-knockdown cells. These findings establish 1110025M09Rik as a protein-coding gene that regulates BMAT development, providing novel insights into the molecular mechanisms of adipogenesis and highlighting potential therapeutic targets for skeletal and metabolic disorders.
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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