Osteoporosis is a prevalent bone metabolic disease characterized by bone fragility. As a key pathophysiological mechanism, the disease is caused by excessive bone resorption (by osteoclasts) over bone formation (by osteoblasts). Peripheral blood monocytes (PBMs) represent a major systemic cell type for bone metabolism by serving as progenitors of osteoclasts and producing cytokines important for osteoclastogenesis. Our lab previously used microarray-based transcriptomics profiling to identify a list of novel genes for osteoporosis.

My work is to further investigate the factors and regulatory network in osteoporosis, using microarray data of monocytes from subjects with extremely high/low hip bone mineral density. 1) We performed a pathway analysis and developed a novel approach to correct the "crosstalk" phenomenon which is caused by overlapping genes. 2) We analyzed the long non-coding RNA (lncRNA) profile by re-annotating exon array and predicted the regulatory mechanism of lncRNAs on protein coding genes in bone metabolism. 3) We identified the important potential transcription factors for osteoporosis and inferred the regulatory mechanism which exists between transcription factors and target genes in bone metabolism.

My findings not only reported the key regulatory factors (lncRNAs and transcriptional factors) contributes to bone metabolism, but also explored the potential regulatory networks in osteoporosis.