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Transcriptome analysis of mouse bone marrow mesenchymal stem cells treated with ellagic acid

ABSTRACT: To investigate the effect of ellagic acid on osteoblast differentiation in mouse bone marrow mesenchymal stem cells, we performed transcriptome analysis，foreseeing a molecular mechanism of ellagic acid-mediated osteoblast differentiation in mouse bone marrow mesenchymal stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE224344 | GEO | 2026/02/12

REPOSITORIES: GEO

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Project description:Background: Gout is an inflammatory arthritis associated with increased bone anabolism and a higher risk of ectopic bone formation. Colchicine, used to prevent and treat acute gouty flares, inhibits microtubule polymerization and has been described to promote osteoblastogenesis. In bone disorders such as osteoporosis, disruption of the osteoblast–adipocyte balance contributes to pathology, yet no therapies directly target bone marrow adiposity. Thus, we decided to investigate the impact of colchicine on the osteoblast-adipocyte balance. Methods: C3H10T1/2 mesenchymal stem cells were differentiated to both cell fates in the presence or absence of colchicine. Differentiation was assessed by studying differentiation phenotypes, as well as adipocytic and osteoblastic marker genes. Disrupting microtubule homeostasis through stathmin (STMN1) silencing was employed to mimic colchicine effects on differentiation. Proteomic analysis was performed to gain further insight into colchicine’s effects on adipogenesis. Results: Colchicine promoted transcriptional changes consistent with osteoblastogenic commitment and inhibited adipogenesis, as evidenced by reduced intracellular lipid accumulation and downregulation of adipogenic marker genes. These effects were observed following both continuous and transient exposure (median fold-change across adipogenic markers 0.41 and 0.59, respectively). Consistent with colchicine-induced microtubules destabilization, microtubule disruption by STMN1 silencing also suppressed adipogenic differentiation (median fold-change = 0.66), suggesting that colchicine’s anti-adipogenic effect may be due to its impact on the cytoskeleton. Conclusions: These findings indicate that colchicine can suppress adipogenic differentiation while favouring osteoblast commitment in mesenchymal stem cells. Although further validation in relevant preclinical models required, its efficacy following transient exposure supports the exploration of site-specific strategies that limit systemic toxicity.

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Transcriptome analysis of mouse bone marrow mesenchymal stem cells treated with ellagic acid

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