MiR-99b-5p suppressed proliferation of human osteoblasts by targeting FGFR3 in osteoporosis

Osteoporosis is a common skeletal disease characterized by reduced bone mass partially caused by an imbalance between bone resorption and formation. Considering the potential role of microRNAs (miRNAs) in osteoporosis, we attempted to identify deregulated miRNA that participates in the pathogenesis...

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Veröffentlicht in:Human cell : official journal of Human Cell Research Society 2021-09, Vol.34 (5), p.1398-1409
Hauptverfasser: Ding, Muliang, Liu, Bo, Chen, Xia, Ouyang, Zhengxiao, Peng, Dan, Zhou, Yu
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container_issue 5
container_start_page 1398
container_title Human cell : official journal of Human Cell Research Society
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creator Ding, Muliang
Liu, Bo
Chen, Xia
Ouyang, Zhengxiao
Peng, Dan
Zhou, Yu
description Osteoporosis is a common skeletal disease characterized by reduced bone mass partially caused by an imbalance between bone resorption and formation. Considering the potential role of microRNAs (miRNAs) in osteoporosis, we attempted to identify deregulated miRNA that participates in the pathogenesis of osteoporosis. We analyzed online datasets for differentially expressed miRNAs and predicted deregulated miRNA target genes, applied these genes for signaling pathway enrichment annotation, and selected the possible miR-99b-5p/FGFR3 axis. Within osteoporosis bone tissues, miR-99b-5p was upregulated and FGFR3 was downregulated. miR-99b-5p overexpression inhibited osteoblast proliferation and osteogenesis-related genes expression, whereas FGFR3 overexpression exerted opposite effects upon the proliferation of osteoblasts and osteogenesis-related genes expression. By direct targeting, miR-99b-5p inhibited FGFR3 expression. Moreover, FGFR3 silencing significantly reversed the roles of miR-99b-5p inhibition in the proliferation of osteoblasts and osteogenesis-related genes expression. In conclusion, we identify a deregulated miRNA/mRNA axis in osteoporosis and osteogenic differentiation, namely the miR-99b-5p/FGFR3 axis; through targeting FGFR3, miR-99b-5p inhibits osteoblast proliferation and activity, which might subsequently affect the bone formation in osteoporosis progression.
doi_str_mv 10.1007/s13577-021-00567-3
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Considering the potential role of microRNAs (miRNAs) in osteoporosis, we attempted to identify deregulated miRNA that participates in the pathogenesis of osteoporosis. We analyzed online datasets for differentially expressed miRNAs and predicted deregulated miRNA target genes, applied these genes for signaling pathway enrichment annotation, and selected the possible miR-99b-5p/FGFR3 axis. Within osteoporosis bone tissues, miR-99b-5p was upregulated and FGFR3 was downregulated. miR-99b-5p overexpression inhibited osteoblast proliferation and osteogenesis-related genes expression, whereas FGFR3 overexpression exerted opposite effects upon the proliferation of osteoblasts and osteogenesis-related genes expression. By direct targeting, miR-99b-5p inhibited FGFR3 expression. Moreover, FGFR3 silencing significantly reversed the roles of miR-99b-5p inhibition in the proliferation of osteoblasts and osteogenesis-related genes expression. 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subjects Aged
Biomedical and Life Sciences
Bone growth
Bone mass
Bone resorption
Cell Biology
Cell Proliferation - genetics
Cells, Cultured
Female
Fibroblast growth factor receptors
Gene Expression - genetics
Gene Expression Regulation, Developmental - genetics
Gene Expression Regulation, Developmental - physiology
Gynecology
Humans
Life Sciences
Male
MicroRNAs
MicroRNAs - physiology
Middle Aged
miRNA
mRNA
Oncology
Osteoblastogenesis
Osteoblasts
Osteoblasts - physiology
Osteogenesis
Osteogenesis - genetics
Osteogenesis - physiology
Osteoporosis
Osteoporosis - genetics
Osteoporosis - pathology
Receptor, Fibroblast Growth Factor, Type 3 - genetics
Receptor, Fibroblast Growth Factor, Type 3 - metabolism
Reproductive Medicine
Research Article
Signal transduction
Signal Transduction - genetics
Signal Transduction - physiology
Stem Cells
Surgery
title MiR-99b-5p suppressed proliferation of human osteoblasts by targeting FGFR3 in osteoporosis
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