Osteoclast-associated receptor blockade prevents articular cartilage destruction via chondrocyte apoptosis regulation
Osteoarthritis (OA), primarily characterized by articular cartilage destruction, is the most common form of age-related degenerative whole-joint disease. No disease-modifying treatments for OA are currently available. Although OA is primarily characterized by cartilage destruction, our understanding of the processes controlling OA progression is poor. Here, we report the association of OA with increased levels of osteoclast-associated receptor (OSCAR), an immunoglobulin-like collagen-recognition receptor. In mice, OSCAR deletion abrogates OA manifestations, such as articular cartilage destruction, subchondral bone sclerosis, and hyaline cartilage loss. These effects are a result of decreased chondrocyte apoptosis, which is caused by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in induced OA. Treatments with human OSCAR-Fc fusion protein attenuates OA pathogenesis caused by experimental OA. Thus, this work highlights the function of OSCAR as a catabolic regulator of OA pathogenesis, indicating that OSCAR blockade is a potential therapy for OA.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
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Enthalten in: |
Nature communications - 11(2020), 1 vom: 28. Aug., Seite 4343 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Park, Doo Ri [VerfasserIn] |
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Links: |
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Themen: |
Journal Article |
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Anmerkungen: |
Date Completed 17.09.2020 Date Revised 28.08.2021 published: Electronic Citation Status MEDLINE |
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doi: |
10.1038/s41467-020-18208-y |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM314331018 |
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520 | |a Osteoarthritis (OA), primarily characterized by articular cartilage destruction, is the most common form of age-related degenerative whole-joint disease. No disease-modifying treatments for OA are currently available. Although OA is primarily characterized by cartilage destruction, our understanding of the processes controlling OA progression is poor. Here, we report the association of OA with increased levels of osteoclast-associated receptor (OSCAR), an immunoglobulin-like collagen-recognition receptor. In mice, OSCAR deletion abrogates OA manifestations, such as articular cartilage destruction, subchondral bone sclerosis, and hyaline cartilage loss. These effects are a result of decreased chondrocyte apoptosis, which is caused by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in induced OA. Treatments with human OSCAR-Fc fusion protein attenuates OA pathogenesis caused by experimental OA. Thus, this work highlights the function of OSCAR as a catabolic regulator of OA pathogenesis, indicating that OSCAR blockade is a potential therapy for OA | ||
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700 | 1 | |a Kim, Gyeong Min |e verfasserin |4 aut | |
700 | 1 | |a Lee, Haeseung |e verfasserin |4 aut | |
700 | 1 | |a Kim, Minhee |e verfasserin |4 aut | |
700 | 1 | |a Hwang, Donghyun |e verfasserin |4 aut | |
700 | 1 | |a Lee, Hana |e verfasserin |4 aut | |
700 | 1 | |a Kim, Han-Sung |e verfasserin |4 aut | |
700 | 1 | |a Kim, Wankyu |e verfasserin |4 aut | |
700 | 1 | |a Park, Min Chan |e verfasserin |4 aut | |
700 | 1 | |a Shim, Hyunbo |e verfasserin |4 aut | |
700 | 1 | |a Lee, Soo Young |e verfasserin |4 aut | |
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