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Primary Cilium, a Potential Target of Microgravity Induced Bone Loss

Wengui Shi 1,2 and Jufang Wang*1

DOI: 10.26717/BJSTR.2017.01.000102

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    Gansu Key laboratory of Space Radiobiology, Institute of Modern Physics, China

    University of Chinese Academy of Sciences, China

    *Corresponding author: Jufang Wang, Gansu Key laboratory of Space Radiobiology, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, PR China

Received: April 11, 2017   Published: May 17, 2017

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Microgravity in space can cause various problems in different biological systems. One of the most prominent and well recognized physiological challenges accompanying an extended spaceflight is the reduction in bone mass [1]. However, the underlying mechanisms of this phenomenon are still elusive. Primary cilium is a solitary and special organelle that emanates from the surface of most mammalian cells, which is anchored to the cell by mother centriole during the interphase and G0 of cell cycle [2]. For a long time, primary cilium was considered as a vestigial organelle. Until recently it was found that primary cilium provided a means of sequestering the centriole, so as to inhibit cell division. More significantly, a variety of receptors, ion channels and transporter proteins have been localized to the cilium, which has been proved as a key coordinator of signaling pathways to respond mechanical and chemical stimuli [3,4]. Primary cilium has been proved as a mechanosensor to regulate bone formation both in osteocytes and osteoblasts. It can act as a sensory organelle to receive extracellular signals and change its orientation to translate mechanical stimuli into biochemical and transcriptional changes, and as a result, bone formation is activated [5,6]. Inspired by established role as a mechanosensor, the role of primary cilium in microgravity induced bone loss must be studied. In here we presents the structure and function of primary cilium in bone metabolism process, and prospects the importance of primary cilia in microgravity stimulated osteoporosis.

Primary Cilium | New Signaling Pathways | Bone Homeostasis | Figures | References