Min Ma1, Shulin Luo1, Wei Zhou1, Liangyu Lu1, Junfeng Cai2, Feng Yuan1, Feng Yin3. 1. Tongji University, Department of Orthopaedic Surgery, Shanghai East Hospital, Shanghai, China. 2. Tongji University, Department of Orthopaedic Surgery, Shanghai East Hospital, Shanghai, China. Electronic address: jjianglei@126.com. 3. Tongji University, Department of Orthopaedic Surgery, Shanghai East Hospital, Shanghai, China. Electronic address: ywindfw@163.com.
Abstract
OBJECTIVE: The aim of this study was to gain a better understanding of the molecular mechanisms and identify more critical genes associated with the pathogenesis of postmenopausal osteoporosis (PMOP). MATERIALS AND METHODS: Microarray data of GSE13850 were download from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified either in B cells from postmenopausal female nonsmokers with high bone mineral density (BMD) compared with those with low BMD (defined as DEG1 group) or in B cells from postmenopausal female smokers with high BMD compared with postmenopausal female nonsmokers with high BMD (defined as DEG2 group). Gene ontology and immune-related functional enrichment analysis of DEGs were performed. Additionally, the protein-protein interaction network of all DEGs was constructed and subnetworks of the hub genes were extracted. RESULTS: A total of 51 DEGs were identified in the DEG1 group, including 30 up- and 21 downregulated genes. Besides, 86 DEGs were identified in the DEG2 group, of which 46 were upregulated and 40 were downregulated. Immune enrichment analysis showed DEGs were mainly enriched in functions of CD molecules and chemokines and receptor, and the upregulated gene interleukin 4 receptor (IL-4R) was significantly enriched. Moreover, guanine nucleotide-binding protein G (GNAI2), filamin A alpha (FLNA), and transforming growth factor-β1 (TGFB1) were hub proteins in the protein-protein interaction network. CONCLUSION: IL-4R, GNAI2, FLNA, and TGFB1 may be potential target genes associated with the pathogenesis of PMOP. In particular, FLNA, and TGFB1 may be affected by smoking, a risk factor of PMOP.
OBJECTIVE: The aim of this study was to gain a better understanding of the molecular mechanisms and identify more critical genes associated with the pathogenesis of postmenopausal osteoporosis (PMOP). MATERIALS AND METHODS: Microarray data of GSE13850 were download from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified either in B cells from postmenopausal female nonsmokers with high bone mineral density (BMD) compared with those with low BMD (defined as DEG1 group) or in B cells from postmenopausal female smokers with high BMD compared with postmenopausal female nonsmokers with high BMD (defined as DEG2 group). Gene ontology and immune-related functional enrichment analysis of DEGs were performed. Additionally, the protein-protein interaction network of all DEGs was constructed and subnetworks of the hub genes were extracted. RESULTS: A total of 51 DEGs were identified in the DEG1 group, including 30 up- and 21 downregulated genes. Besides, 86 DEGs were identified in the DEG2 group, of which 46 were upregulated and 40 were downregulated. Immune enrichment analysis showed DEGs were mainly enriched in functions of CD molecules and chemokines and receptor, and the upregulated gene interleukin 4 receptor (IL-4R) was significantly enriched. Moreover, guanine nucleotide-binding protein G (GNAI2), filamin A alpha (FLNA), and transforming growth factor-β1 (TGFB1) were hub proteins in the protein-protein interaction network. CONCLUSION:IL-4R, GNAI2, FLNA, and TGFB1 may be potential target genes associated with the pathogenesis of PMOP. In particular, FLNA, and TGFB1 may be affected by smoking, a risk factor of PMOP.