Interaction between circadian gene Bmal1 and adipogenic regulator PPARγ in UVB-exposed mesenchymal stem cells
Abstract
Background: Mesenchymal stem cells (MSCs), including adipose-derived MSCs (ADMSCs) and bone marrow-derived MSCs (BMMSCs), are multipotent cells essential for tissue repair, with strong self-renewal and differentiation abilities. Bmal1 is a core component of the circadian cycle and plays a regulatory role in stem cell specialization; PPARγ links adipogenesis to the circadian rhythm by epigenetically regulating Bmal1. Ultraviolet B (UVB) radiation influences circadian processes by modulating the expression of growth factors and cytokines in MSCs.
Aims: This study investigated how UVB affects adipogenesis and circadian-system-related gene transcription in ADMSCs and BMMSCs.
Methods: MSC viability post-exposure was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis. Cells were cultured in adipogenesis medium and stained with Oil Red O at multiple time points. UVB-treated MSCs were maintained under differentiation-inducing conditions for 28 days, and gene expression was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR).
Results: Viability assays identified 25 mJ/cm² as the optimal UVB dose. Flow cytometry confirmed the enhanced expression of MSC markers (CD54, CD90, and CD29) and low expression of hematopoietic markers (CD45, CD106, and MHC class II). Oil Red O staining revealed gradual lipid accumulation, beginning on day 14 and forming mature droplets by day 28. qRT-PCR indicated a significant increase in PPARγ expression in adipogenic differentiation groups and Bmal1 expression post-UVB exposure.
Conclusion: Overall, these findings suggest that UVB stimulation at optimal doses enhances the adipogenic differentiation capacity of MSCs while modulating circadian rhythm-associated genes. Moreover, adipogenic differentiation itself appears to contribute to the regulation of the circadian rhythm.
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Details
Primary Language
English
Subjects
Cell Metabolism
Journal Section
Research Article
Publication Date
July 9, 2026
Submission Date
December 2, 2025
Acceptance Date
March 20, 2026
Published in Issue
Year 2026 Volume: 27 Number: 1
