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Analysis of differential genes in osteogenic induction of alveolar bone derived MSCs under TNFα-induced inflammation in Ccrl2-KO mice and WT mice.

ABSTRACT: In order to explore the effect of Ccrl2 knockout on the osteogenic differentiation of MSCs under inflammatory conditions, MSCs derived from the alveolar bones of Ccrl2-KO mice and WT mice were extracted, and total cellular RNA was extracted after 2 days of osteogenic induction under TNFα-induced inflammation, and carried out RNA-Seq to identify the potential mechanism by which Ccrl2 regulates osteogenic-related signals.

ORGANISM(S): Mus musculus

PROVIDER: GSE248831 | GEO | 2025/07/31

REPOSITORIES: GEO

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Project description:The intriThe intricate balance between MSCs differentiation to osteoblasts or adipocytes is finely regulated. To explore novel participating molecules, we screened for early-stage osteogenesis- or adipogenesis-based MSCs protein expression profile using TMT-based quantitative proteomic analysis. Protein annotation, hierarchical clustering, functional stratification, and protein-protein association assessments were performed. Moreover, two upregulated proteins, namely, FBLN2 and NPR3, were validated to participate in the osteogenic differentiation process of MSCs. Subsequently, we independently downregulated FBLN2 and NPR3 during 7 days of osteogenic differentiation, and conducted quantitative proteomics analysis to assess the differential protein regulation between knockdown and control cells. Based on gene ontology (GO) and network analyses, FBLN2 deficiency induced functional alterations associated with biological regulation and stimulus response, whereas, NPR3 deficiency induced functional alterations related to cellular and metabolic processes, and so on. These results demonstrated that proteomics is still an effective tool for the comprehensive exploration of the MSCs differentiation process. cate balance between MSCs differentiation to osteoblasts or adipocytes is finely regulated. To explore novel participating molecules, we screened for early-stage osteogenesis- or adipogenesis-based MSCs protein expression profile using TMT-based quantitative proteomic analysis. Protein annotation, hierarchical clustering, functional stratification, and protein-protein association assessments were performed. Moreover, two upregulated proteins, namely, FBLN2 and NPR3, were validated to participate in the osteogenic differentiation process of MSCs. Subsequently, we independently downregulated FBLN2 and NPR3 during 7 days of osteogenic differentiation, and conducted quantitative proteomics analysis to assess the differential protein regulation between knockdown and control cells. Based on gene ontology (GO) and network analyses, FBLN2 deficiency induced functional alterations associated with biological regulation and stimulus response, whereas, NPR3 deficiency induced functional alterations related to cellular and metabolic processes, and so on. These results demonstrated that proteomics is still an effective tool for the comprehensive exploration of the MSCs differentiation process.

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Analysis of differential genes in osteogenic induction of alveolar bone derived MSCs under TNFα-induced inflammation in Ccrl2-KO mice and WT mice.

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