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PIP5k1 β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation

Xiaoying Zhao, Guoli Hu, Chuandong Wang, Lei Jiang, Jingyu Zhao, Jiake Xu, Xiaoling Zhang
doi: https://doi.org/10.1101/288910
Xiaoying Zhao
1Department of Orthopedic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China
2The Key Laboratory of Stem Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China
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Guoli Hu
1Department of Orthopedic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China
2The Key Laboratory of Stem Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China
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Chuandong Wang
1Department of Orthopedic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China
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Lei Jiang
4Key laboratory of Tibetan medicine research, Northwest Plateau Institute of Biology, Chinese Academy of Sciences, Xining 810001, PR China
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Jingyu Zhao
1Department of Orthopedic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China
2The Key Laboratory of Stem Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China
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Jiake Xu
3School of Pathology and Laboratory Medicine, University of Western Australia, Perth, Western Australia, 6009, Australia
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Xiaoling Zhang
1Department of Orthopedic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China
2The Key Laboratory of Stem Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China
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  • For correspondence: xlzhang@shsmu.edu.cn
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Abstract

PIP5K1β is crucial to generation of phosphotidylinosotol (4, 5) P2. PIP5K1β participates in numerous cellular activities, such as B cell and platelet activation, cell phagocytosis and endocytosis, cell apoptosis, and cytoskeletal organization. In the present work, we aimed to make insight into the function of PIP5K1β in osteoclastogenesis and osteogenesis to provide promising strategies for osteoporosis prevention and treatment. We discovered that PIP5k1β deletion in mice resulted in obvious bone loss and PIP5K1β was highly expressed both during osteoclast and osteoblast differentiation, besides, PIP5K1β deletion enhanced the proliferation and migration of BMMs to promote osteoclast differentiation. PIP5k1β−/− osteoclast exhibited normal cytoskeleton architecture but stronger resorption activity. PIP5k1β deficiency also promoted activation of MAPK and Akt signaling, enhanced TRAF6 and c-Fos expression, facilitated the expression and nuclear translocation of NFATC1 and upregulated Grb2 expression, thereby accelerating osteoclast differentiation and function. Finally, PIP5K1β enhanced osteoblast differentiation by upregulating master genes expression through triggering smad1/5/8 signaling. Thereby, PIP5K1β modulate bone homeostasis and remodeling.

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Posted March 26, 2018.
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PIP5k1 β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation
Xiaoying Zhao, Guoli Hu, Chuandong Wang, Lei Jiang, Jingyu Zhao, Jiake Xu, Xiaoling Zhang
bioRxiv 288910; doi: https://doi.org/10.1101/288910
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PIP5k1 β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation
Xiaoying Zhao, Guoli Hu, Chuandong Wang, Lei Jiang, Jingyu Zhao, Jiake Xu, Xiaoling Zhang
bioRxiv 288910; doi: https://doi.org/10.1101/288910

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