한빛사논문
- 조회1,358
Hyo Jung Sim1,†, Chanmi Cho2,3,4,5,†, Ha Eun Kim1, Ju Yeon Hong1, Eun Kyung Song1, Keun Yeong Kwon1, Dong Gil Jang1, Seok-Jung Kim6, Hyun-Shik Lee7, Changwook Lee1, Taejoon Kwon1,8, Siyoung Yang2,3,4,5,*, Tae Joo Park1,8,*
1School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Korea. 2Department of Pharmacology, Ajou University School of Medicine, Suwon 16499, Korea. 3Department of Biomedical Sciences, Graduate School, Ajou University, Suwon 16499, Korea. 4CIRNO, Sungkyunkwan University, Suwon 16419, Korea. 5Degenerative Inter Diseases Research Center, Ajou University School of Medicine, Suwon 16499, Korea. 6Department of Orthopaedic Surgery, Uijeongbu St. Mary’s Hospital, Catholic University of Korea College of Medicine, Uijeongbu 11765, Korea. 7BK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea. 8Center for Genomic Integrity, Institute for Basic Science, Ulsan 44919, Korea.
*Corresponding author.
†These authors contributed equally to this work.
Abstract
Chondrocytes secrete massive extracellular matrix (ECM) molecules that are produced, folded, and modified in the endoplasmic reticulum (ER). Thus, the ER-associated degradation (ERAD) complex-which removes misfolded and unfolded proteins to maintain proteostasis in the ER- plays an indispensable role in building and maintaining cartilage. Here, we examined the necessity of the ERAD complex in chondrocytes for cartilage formation and maintenance. We show that ERAD gene expression is exponentially increased during chondrogenesis, and disruption of ERAD function causes severe chondrodysplasia in developing embryos and loss of adult articular cartilage. ERAD complex malfunction also causes abnormal accumulation of cartilage ECM molecules and subsequent chondrodysplasia. ERAD gene expression is decreased in damaged cartilage from patients with osteoarthritis (OA), and disruption of ERAD function in articular cartilage leads to cartilage destruction in a mouse OA model.
논문정보
- Research article
- 2022년 01월 (BRIC 등록일 2022-02-10)
- 국내 연구진
- 생명과학 > 발생생물학
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