Oxysterol 25-hydroxycholesterol as a metabolic pathophysiological factors of osteoarthritis induces apoptosis in primary rat chondrocytes
10.4196/kjpp.2020.24.3.249
- Author:
Yo-Seob SEO
1
;
In-A CHO
;
Tae-Hyeon KIM
;
Jae-Seek YOU
;
Ji-Su OH
;
Gyeong-Je LEE
;
Do Kyung KIM
;
Jae-Sung KIM
Author Information
1. Department of Oral and Maxillofacial Radiology, School of Dentistry, Chosun University, Gwangju 61452, Korea
- Publication Type:Original Article
- From:The Korean Journal of Physiology and Pharmacology
2020;24(3):249-257
- CountryRepublic of Korea
- Language:English
-
Abstract:
The aim of the present study was to investigate the pathophysiological etiology of osteoarthritis that is mediated by the apoptosis of chondrocytes exposed to 25-hydroxycholesterol (25-HC), an oxysterol synthesized by the expression of cholesterol-25-hydroxylase (CH25H) under inflammatory conditions. Interleukin-1β induced the apoptosis of chondrocytes in a dose- dependent manner. Furthermore, the production of 25-HC increased in the chondrocytes treated with interleukin-1β through the expression of CH25H. 25-HC decreased the viability of chondrocytes. Chondrocytes with condensed nucleus and apoptotic populations increased by 25- HC. Moreover, the activity and expression of caspase-3 were increased by the death ligand-mediated extrinsic and mitochondria-dependent intrinsic apoptotic pathways in the chondrocytes treated with 25-HC. Finally, 25-HC induced not only caspasedependent apoptosis, but also induced proteoglycan loss in articular cartilage ex vivo cultured rat knee joints. These data indicate that 25-HC may act as a metabolic pathophysiological factor in osteoarthritis that is mediated by progressive chondrocyte death in the articular cartilage with inflammatory condition.
