Abstract
During the aging process, impaired osteoblastic function is one key factor of imbalanced bone formation and age-related bone loss. The aim of this study is to explore the differentially expressed genes in normal and aged osteoblasts and to identify genes potentially involved in age-related alteration in bone physiology. Based on next generation sequencing and bioinformatics analysis, 12 differentially expressed microRNAs and 22 differentially expressed genes were identified. Up-regulation of miR-204-5p was validated in an array of osteoporotic hip fracture in the Gene Expression Omnibus database (GSE74209). The putative targets for miR-204-5p were Kruppel-like factor 7 (KLF7) and SRY-box 11 (SOX11). Ingenuity Pathway Analysis identified SOX11, involved in osteoarthritis pathway and differentiation of osteoblasts, together with miR-204-5p, a potential upstream regulator, suggesting the critical role of miR-204-5p-SOX11 regulation in the aging process of human bones. In addition, as semaphorin 3A (SEMA3A) and ephrin type-A receptor 5 (EPHA5) were involved in nervous system related biological functions, we postulated a potential linkage between SEMA3A, EPHA5 and development of neurogenic heterotopic ossification. Our findings implicate new candidate genes in the diagnosis of geriatric musculoskeletal disorders, and provide novel insights that may contribute to the elaboration of new biomarkers for neurogenic heterotopic ossification.
Highlights
Life expectancy has increased during the past decades, and issues related to global aging are growing
Bone structure consists of trabecular bone and cortical bone
As the osteoblasts were cultured to later passages, the cell morphologies changed from thin, spindle shape to flattened, irregular shape with increased intracellular debris (Figure 1A)
Summary
Life expectancy has increased during the past decades, and issues related to global aging are growing. Bone structure consists of trabecular bone and cortical bone. Trabecular bone is more metabolically active and its bone mineral density begins to decrease in young adulthood. Cortical bone provides mainly structural support, and its bone mineral density remains stable until middle age and begins to decrease [3]. Postmenopausal increase in bone turnover and bone porosity is the primary factor for women having more overall cortical bone loss than men throughout life [4]. Osteoblasts are responsible for bone formation, whereas osteoclasts are responsible for bone resorption [5]. Disequilibrium of osteoblast and osteoclast activities related to aging, metabolic diseases and hormonal changes may lead to bone fragility and clinical disorders such as osteoporosis [6]
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