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Selective regulation of osteoclast adhesion and spreading by PLCャ/PKCメ-PKCヤ/RhoA-Rac1 signaling
Jin-Man Kim1,2,#, Kyunghee Lee1,#, Daewon Jeong1,*
1Department of Microbiology, Laboratory of Bone Metabolism and Control, Yeungnam University College of Medicine,
2Asan Medical Center, Asan Institute for Life Sciences
Bone resorption by multinucleated osteoclasts is a multistep process involving adhesion to the bone matrix, migration to resorption sites, and formation of sealing zones and ruffled borders. Macrophage colony-stimulating factor (M-CSF) and osteopontin (OPN) have been shown to be involved in the bone resorption process by respective activation of integrin メvモ3 via “inside-out” and “outside-in” signaling. In this study, we investigated the link between signal modulators known to M-CSF- and OPN-induced osteoclast adhesion and spreading. M-CSF- and OPN-induced osteoclast adhesion was achieved via activation of stepwise signals, including integrin メvモ3, PLCャ, PKCヤ, and Rac1. Osteoclast spreading induced by M-CSF and OPN was shown to be controlled via sequential activation, consistent with the osteoclast adhesion processes. In contrast to osteoclast adhesion, osteoclast spreading induced by M-CSF and OPN was blocked via activation of PLCャ/PKCメ/RhoA signaling. The combined results indicate that osteoclast adhesion and spreading are selectively regulated via PLCャ/PKCメ-PKCヤ/RhoA-Rac1 signaling.
Abstract, Accepted Manuscript(in press) [Submitted on October 17, 2017, Accepted on December 4, 2017]
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