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Biochem Biophys Res Commun. 2018 Mar 11;497(3):890-896. doi: 10.1016/j.bbrc.2018.02.164. Epub 2018 Feb 21.

IL-17A regulates the autophagic activity of osteoclast precursors through RANKL-JNK1 signaling during osteoclastogenesis in vitro.

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Shengli Clinical Medical College of Fujian Medical University, No. 134Dong Jie Road, Fuzhou 350001, China.
Pediatrics Department, Division of Metabolism and Endocrinology, John Hopkins University, Baltimore, MD, USA.
Shengli Clinical Medical College of Fujian Medical University, No. 134Dong Jie Road, Fuzhou 350001, China; Endocrinology Department, Fujian Provincial Hospital, No. 134Dong Jie Road, Fuzhou 350001, China. Electronic address:


Interleukin-17A(IL-17A), a proinflammatory cytokine, may have effects on osteoclastic resorption in inflammation-mediated bone loss, including postmenopausal osteoporosis. IL-17A could alter autophagic activity among other tissues and cells, thereby causing corresponding lesions. The aim of this study was to clarify how IL-17A influenced osteoclastogenesis by regulating autophagy. The present study showed that IL-17A could facilitate osteoclast precursors (OCPs) autophagy and osteoclastogenesis at a low concentration. Furthermore, suppression of autophagy with chloroquine (CQ) or 3-MA could significantly attenuate the enhanced osteoclastogenesis by a low level of IL-17A. It was also found that a low level of IL-17A couldn't up-regulate OCPs autophagy after removal of RANKL(Receptor Activator for Nuclear Factor-κB Ligand), and JNK(c-Jun N-terminal kinase) inhibitor only inhibited autophagy at a low level of IL-17A. These results suggest that a low concentration of IL-17A is likely to promote autophagic activity via activating RANKL-JNK pathway during osteoclastogenesis.


Autophagy; IL-17A; JNK; Osteoclast; RANKL

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