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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.

Author information

1
Shengli Clinical Medical College of Fujian Medical University, No. 134Dong Jie Road, Fuzhou 350001, China.
2
Pediatrics Department, Division of Metabolism and Endocrinology, John Hopkins University, Baltimore, MD, USA.
3
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: hjm996@126.com.

Abstract

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.

KEYWORDS:

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

PMID:
29476739
DOI:
10.1016/j.bbrc.2018.02.164
[Indexed for MEDLINE]

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