The novel tRF-23 promotes osteogenic differentiation of hBMSCs and protects against bone loss in ovariectomized mice
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ABSTRACT:
PROVIDER: PRJNA1311110 | ENA |
REPOSITORIES: ENA
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Project description:The pathogenesis of osteoporosis is closely related to the impaired human bone marrow-derived stromal cells (hBMSCs) osteogenic differentiation. No studies to date, however, have established whether tRNA-derived fragments (tRFs) can influence osteogenic differentiation of hBMSCs or the onset of osteoporosis. Here, tRF-23 was found to control hBMSC osteogenesis through its ability to target suppressor of cytokine signaling 1 (SOCS1) via the Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3) signaling pathway. tRF-23 was then further established as a potential target for efforts to protect against bone loss and marrow adipose tissue (MAT) accumulation in osteoporotic model mice, and its molecular mechanism was also verified in vivo. Together, these results suggest a model in which tRF-23 can protect against bone loss induced by ovariectomized (OVX) through the augmentation of hBMSC osteogenesis, providing a foundation for further characterizing the pathogenesis of osteoporosis and seeking new therapeutic targets for this disruptive condition.
2026-01-19 | PXD067728 | Pride
Project description:The pathogenesis of osteoporosis is closely related to the impaired human bone marrow-derived stromal cells (hBMSCs) osteogenic differentiation. No studies to date, however, have established whether tRNA-derived fragments (tRFs) can influence osteogenic differentiation of hBMSCs or the onset of osteoporosis. Here, tRF-23 was found to control hBMSC osteogenesis through its ability to target suppressor of cytokine signaling 1 (SOCS1) via the Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3) signaling pathway. tRF-23 was then further established as a potential target for efforts to protect against bone loss and marrow adipose tissue (MAT) accumulation in osteoporotic model mice, and its molecular mechanism was also verified in vivo. Together, these results suggest a model in which tRF-23 can protect against bone loss induced by ovariectomized (OVX) through the augmentation of hBMSC osteogenesis, providing a foundation for further characterizing the pathogenesis of osteoporosis and seeking new therapeutic targets for this disruptive condition.
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Project description:Background: Human bone marrow mesenchymal stromal cells (hBMSCs) are multipotent stromal cells capable of osteogenic differentiation, making them a promising cell source for bone tissue engineering and regenerative medicine. Identifying key factors that regulate hBMSCs osteogenic differentiation is crucial for enhancing bone regeneration strategies. Objective: This study aims to identify target genes underlying impaired osteogenic differentiation of hBMSCs under oxidative stress (OS) through integrated transcriptomic and proteomic approaches, and delineate the role of proenkephalin (PENK) in this process. Methods: OS model and impaired osteogenic differentiation model were established in hBMSCs using hydrogen peroxide (H2O2). Cellular oxidative stress levels were assessed using Dihydroethidium (DHE) fluorescent probes and JC-1 staining. Osteogenic differentiation was evaluated by alkaline phosphatase (ALP) activity and Alizarin Red staining (ARS). Key genes and proteins were predicted via integrated transcriptomic and proteomic analyses. The role of PENK in osteogenic differentiation was validated using lentiviral transfection. Results: This study established 400 μM H2O2 as the optimal concentration for inducing impaired osteogenic differentiation in hBMSCs. Integrated transcriptomic and proteomic analysis identified 18 pivotal regulatory genes that orchestrate impaired osteogenic differentiation of hBMSCs under OS. Among these, PENK was identified as a potential therapeutic target involved in regulating oxidative stress-impaired osteogenic differentiation of hBMSCs. Functional validation confirmed that PENK overexpression promotes osteogenic differentiation in hBMSCs. Conclusion: OS contributes to impaired osteogenic differentiation in hBMSCs. PENK regulates osteogenic differentiation of hBMSCs under OS and holds promise as a novel therapeutic target for bone regeneration and repair.
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Project description:Background: Human bone marrow mesenchymal stromal cells (hBMSCs) are multipotent stromal cells capable of osteogenic differentiation, making them a promising cell source for bone tissue engineering and regenerative medicine. Identifying key factors that regulate hBMSCs osteogenic differentiation is crucial for enhancing bone regeneration strategies. Objective: This study aims to identify target genes underlying impaired osteogenic differentiation of hBMSCs under oxidative stress (OS) through integrated transcriptomic and proteomic approaches, and delineate the role of proenkephalin (PENK) in this process. Methods: OS model and impaired osteogenic differentiation model were established in hBMSCs using hydrogen peroxide (H2O2). Cellular oxidative stress levels were assessed using Dihydroethidium (DHE) fluorescent probes and JC-1 staining. Osteogenic differentiation was evaluated by alkaline phosphatase (ALP) activity and Alizarin Red staining (ARS). Key genes and proteins were predicted via integrated transcriptomic and proteomic analyses. The role of PENK in osteogenic differentiation was validated using lentiviral transfection. Results: This study established 400 μM H2O2 as the optimal concentration for inducing impaired osteogenic differentiation in hBMSCs. Integrated transcriptomic and proteomic analysis identified 18 pivotal regulatory genes that orchestrate impaired osteogenic differentiation of hBMSCs under OS. Among these, PENK was identified as a potential therapeutic target involved in regulating oxidative stress-impaired osteogenic differentiation of hBMSCs. Functional validation confirmed that PENK overexpression promotes osteogenic differentiation in hBMSCs. Conclusion: OS contributes to impaired osteogenic differentiation in hBMSCs. PENK regulates osteogenic differentiation of hBMSCs under OS and holds promise as a novel therapeutic target for bone regeneration and repair.
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Project description:Nanotopographic cues from biomaterials exert powerful effects on the osteogenic differentiation of mesenchymal stem cells because of their niche-mimicking features. However, the biological mechanisms underlying cell lineage determination by surface nanotopography have not been clearly elucidated. Here, we explored the osteogenic behavior of human bone marrow mesenchymal stem cells (hBMSCs) on PLLA nanofibers with different orientations, and monitored the dynamic changes in global gene expression triggered by topographical cues.
2014-09-01 | GSE48616 | GEO
Project description:In this study, we performed the high-throughput sequencing of hBMSCs between day 0 and day 21 during induction of osteogenic differentiation, followed by analysis of the different expression in whole transcriptomes.
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Project description:Pathological processes like osteoporosis or steroid-induced osteonecrosis of the hip are accompanied by increased bone marrow adipogenesis. Such disorder of adipogenic/osteogenic differentiation, which affects also bone marrow derived mesenchymal stem cells (BMSCs) contributes to bone loss during aging. Therefore, we investigated the effects of extracellular vesicles (EVs) isolated from human (h)BMSCs during different stages of osteogenic differentiation on osteogenic and adipogenic differentiation capacity of naïve hBMSCs.
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