Abstract:
:Cytoplasmic polyadenylation element binding (CPEB) proteins are RNA-binding proteins involved in translational regulation of the specific target mRNAs and control function of various organs including brain, liver and hematopoietic system. However, the role of CPEB proteins during osteoclast differentiation remains unclear. Here we show that Cpeb4 is required for RANKL-induced osteoclast differentiation in mouse macrophage-derived RAW264.7 cell line. Cpeb4 mRNA and protein levels are upregulated at the late stage of osteoclast differentiation. Immunofluorescence analysis revealed that Cpeb4 is translocated from cytoplasm to nuclear bodies in response to RANKL stimulation. Inhibition of PI3K-Akt signaling or calcium-NFAT pathways using chemical inhibitors suppressed nuclear localization of Cpeb4. Loss-of-function analysis showed that shRNA-mediated Cpeb4 depletion strongly impaired TRAP-positive osteoclast formation and expression of key differentiation markers including Acp5, Ctsk, Nfatc1 and Dcstamp. These results suggest that Cpeb4 is a positive regulator in osteoclastogenesis downstream of RANKL signaling.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Arasaki Y,Li M,Akiya T,Nozawa I,Ezura Y,Hayata Tdoi
10.1016/j.bbrc.2020.05.089subject
Has Abstractpub_date
2020-08-06 00:00:00pages
621-627issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(20)31010-Xjournal_volume
528pub_type
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