Korean J Physiol Pharmacol.  2020 May;24(3):249-257. 10.4196/kjpp.2020.24.3.249.

Oxysterol 25-hydroxycholesterol as a metabolic pathophysiological factors of osteoarthritis induces apoptosis in primary rat chondrocytes

Affiliations
  • 1Department of Oral and Maxillofacial Radiology, School of Dentistry, Chosun University, Gwangju 61452, Korea
  • 2Department of Institute of Dental Science, School of Dentistry, Chosun University, Gwangju 61452, Korea
  • 3Departments of Oral and Maxillofacial Surgery, School of Dentistry, Chosun University, Gwangju 61452, Korea
  • 4Departments of Prosthodontics, School of Dentistry, Chosun University, Gwangju 61452, Korea

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.

Keyword

Apoptosis; Cholesterol; Chondrocytes; Osteoarthritis; 25-Hydroxycholesterol
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