AI Article Synopsis
- The study investigates how different stages of osteoclast precursors migrate, particularly focusing on the role of M-CSF and osteopontin.
- The migration of osteoclastic cells was shown to be regulated by integrin αvβ3 and involves specific signaling pathways (PI3K/PKCα/RhoA and PI3K/PKCδ/Rac1).
- RhoA and Rac1 inactivation specifically affects migration of preosteoclasts and mature osteoclasts, indicating a more complex and differentiated reliance on signaling as osteoclasts mature.
Article Abstract
Cell migration during specialized stages of osteoclast precursors, mononuclear preosteoclasts, and multinucleated mature osteoclasts remain uncertain. M-CSF- and osteopontin-induced osteoclastic cell migration was inhibited by function-blocking monoclonal antibodies specific to the integrin αv and β3 subunits, suggesting that integrin αvβ3 mediates migratory signaling induced by M-CSF and osteopontin. M-CSF and osteopontin stimulation was shown to regulate two branched signaling processes, PI3K/PKCα/RhoA axis and PI3K/PKCδ/Rac1 axis. Interestingly, inactivation of RhoA or Rac1 blocked preosteoclast and mature osteoclast migration but not osteoclast precursor migration in a transwell-based cell migration assay. Moreover, the inhibitory effect on preosteoclast and mature osteoclast migration induced by Rac1 inactivation was more effective than that by RhoA inactivation. Collectively, our findings suggest that osteoclast precursor migration depends on PI3K/PKCα-PKCδ signaling mediated via integrin αvβ3 bypassing RhoA and Rac1, whereas preosteoclast and mature osteoclast migration relies on PI3K/PKCα-PKCδ/RhoA-Rac1 axis signaling mediated via integrin αvβ3 with increased dependency on PKCδ/Rac1 signaling route as differentiation progresses.
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| http://dx.doi.org/10.1016/j.mce.2016.08.042 | DOI Listing |
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