ArticlePloS one2026
Decreased expression of Ly-1 antibody reactive clone (Lyar) triggers enhanced adipogenesis of bone marrow mesenchymal stromal cells in aged bone marrow.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Accumulation of adipocytes within the bone marrow is a frequently observed during aging. However, the molecular mechanisms underlying aberrant adipocyte differentiation in aged bone marrow remain largely unclear. In this study, we identified Ly-1 antibody reactive clone (Lyar) as an interacting partner of TGF-β activated kinase 1 (Tak1), a key molecule of non-canonical TGF-β signaling, through a proteomics approach, and demonstrated its involvement in the regulation of aging-related enhancement of adipogenesis. Lyar was not only implicated in the regulation of BMMSC proliferation but also may partly mediate the inhibitory effects of Bromodomain-containing protein 2 (Brd2). An age-associated decline in Lyar expression was associated with a reduction in FGF2-PI3K-Akt1 signaling activity in aged bone marrow. These findings suggest that Lyar may act as a context-dependent modulator of TGF-β signaling and may be involved in regulating proliferation and differentiation in BMMSCs. The age-related loss of Lyar may contribute to the complex mechanisms underlying enhanced adipogenesis in aged bone marrow, providing new insights into the regulation of mesenchymal stem cell fate during aging.
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