Bioinformatics analysis of gene expression profile in callus tissues of osteoporotic phenotype mice induced by osteoblast‐specific Krm2 overexpression. (1st March 2016)

• Record Type: Journal Article
• Authors: Wang, Chengxue; Yu, Tiecheng; Tan, Lei; Cheng, Jieping
• Is Part Of: International journal of rheumatic diseases. Volume 19:Number 12(2016)
• Page Start: 1263
• Page End: 1271
• Publication Date: 2016-03-01
• Subjects: fracture healing -- hub gene -- molecular mechanism -- osteoporotic mice -- pathway; Rheumatology -- Periodicals; Rheumatology -- Asia -- Periodicals; Rheumatology -- Pacific Area -- Periodicals; Rheumatic Diseases -- Periodicals; Connective Tissue Diseases -- Periodicals; Immune System Diseases -- Periodicals; 616.723
• DOI: 10.1111/1756-185X.12840
• Languages: English
• ISSNs: 1756-1841

Abstract

Abstract: Purpose: The aim of this study was to explore the molecular mechanism of fracture healing in osteoporotic mice. Methods: The gene expression profiles of callus tissues of osteoporotic mice and controls were obtained from Gene Expression Omnibus database. The differentially expressed genes (DEGs) and their related biological function and pathways were investigated. In addition, the protein–protein interaction (PPI) network was constructed for DEG encoding proteins and the differentially expressed transcriptional factor was screened. Results: There were 275 up‐regulated genes and 347 down‐regulated genes. The collagen metabolic process biological function was significantly enriched by down‐regulated genes. Extracellular matrix (ECM)‐receptor interaction was a significant pathway that was enriched by differentially expressed genes. In PPI (protein–protein interaction) network, Pcna was the significant node with highest connective degrees. Other hub nodes, such as Ccnb2 and Rrm2, were closely associated with the p53 signaling pathway. Tal1 and Smad6 were found to be differentially expressed transcription factors. Conclusion: The dysregulated collagen metabolic process, ECM‐receptor interaction and p53 signaling pathway may be responsible for impaired fracture healing of osteoporotic mice. The hub nodes (such as Ccnb2 and Rrm2) and differentially expressed TFs (such as Tal1 and Smad6) play a critical role in bone remodeling of osteoporotic individuals.