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Title: Actin-binding protein coronin 1A controls osteoclastic bone resorption by regulating lysosomal secretion of cathepsin K
Authors: Ohmae, Saori
Noma, Naruto
Toyomoto, Masayasu  kyouindb  KAKEN_id
Shinohara, Masahiro
Takeiri, Masatoshi
Fuji, Hiroaki
Takemoto, Kenji
Iwaisako, Keiko
Fujita, Tomoko
Takeda, Norihiko
Kawatani, Makoto
Aoyama, Mineyoshi
Hagiwara, Masatoshi  kyouindb  KAKEN_id
Ishihama, Yasushi  kyouindb  KAKEN_id  orcid (unconfirmed)
Asagiri, Masataka
Author's alias: 豊本, 雅靖
祝迫, 恵子
藤田, 智子
萩原, 正敏
石濱, 泰
朝霧, 成挙
Keywords: Lysosomes
Issue Date: 16-Mar-2017
Publisher: Springer Nature
Journal title: Scientific reports
Volume: 7
Thesis number: 41710
Abstract: Osteoclasts degrade bone matrix proteins via the secretion of lysosomal enzymes. However, the precise mechanisms by which lysosomal components are transported and fused to the bone-apposed plasma membrane, termed ruffled border membrane, remain elusive. Here, we identified coronin 1A as a negative regulator of exocytotic release of cathepsin K, one of the most important bone-degrading enzymes in osteoclasts. The modulation of coronin 1A expression did not alter osteoclast differentiation and extracellular acidification, but strongly affected the secretion of cathepsin K and osteoclast bone-resorption activity, suggesting the coronin 1A-mediated regulation of lysosomal trafficking and protease exocytosis. Further analyses suggested that coronin 1A prevented the lipidation-mediated sorting of the autophagy-related protein LC3 to the ruffled border and attenuated lysosome–plasma membrane fusion. In this process, the interactions between coronin 1A and actin were crucial. Collectively, our findings indicate that coronin 1A is a pivotal component that regulates lysosomal fusion and the secretion pathway in osteoclast-lineage cells and may provide a novel therapeutic target for bone diseases.
Rights: © The Author(s) 2017 This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
DOI(Published Version): 10.1038/srep41710
PubMed ID: 28300073
Appears in Collections:Journal Articles

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