한빛사논문
- 조회1,101
Sujeong Park1, In-Jeoung Baek2, Ji Hyun Ryu3, Churl-Hong Chun4 & Eun-Jung Jin1,*
1Department of Biological Sciences, College of Natural Sciences, Wonkwang University, Iksan, Chunbuk 54538, Korea. 2Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul 05505, Republic of Korea. 3Department of Carbon Convergence Engineering, Wonkwang University, Iksan, Chunbuk 54538, Korea. 4Department of Orthopedic Surgery, Wonkwang University School of Medicine, Iksan, Chunbuk 54538, Korea.
*Correspondence to Eun-Jung Jin.
Abstract
Here, in Ppara−/− mice, we found that an increased DNL stimulated the cartilage degradation and identified ACOT12 as a key regulatory factor. Suppressed level of ACOT12 was observed in cartilages of OA patient and OA-induced animal. To determine the role and association of ACOT12 in the OA pathogenesis, we generated Acot12 knockout (KO) (Acot12−/−) mice using RNA-guided endonuclease. Acot12−/− mice displayed the severe cartilage degradation with the stimulation of matrix MMPs and chondrocyte apoptosis through the accumulation of acetyl CoA. Delivery of acetyl CoA-conjugated chitosan complex into cartilage stimulated DNL and cartilage degradation. Moreover, restoration of ACOT12 into human OA chondrocytes and OA-induced mouse cartilage effectively rescued the pathophysiological features of OA by regulating DNL. Taken together, our study suggested ACOT12 as a novel regulatory factor in maintaining cartilage homeostasis and targeting ACOT12 could contribute to developing a new therapeutic strategy for OA.
논문정보
- Research article
- 2022년 01월 (BRIC 등록일 2022-02-18)
- 국내 연구진
- 생명과학 > 세포생물학
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