Dietary fat-associated osteoarthritic chondrocytes gain resistance to lipotoxicity through PKCK2/STAMP2/FSP27

• DOI: 10.1038/s41413-018-0020-0
• Publication Date: 2018-07-04T22:37:25Z
• Authors: Sung Won Lee; Jee Hyun Rho; Sang Yeob Lee; Won Tae Chung; Yoo Jin Oh; Jung Ha Kim; Seung Hee Yoo; Woo Young Kwon; Ju Yong Bae; Su Young Seo; Hokeun Sun; Hye Young Kim; Young Hyun Yoo
• Keywords: Lipotoxicity

Free fatty acids (FFAs), which are elevated with metabolic syndrome, considered the principal offender exerting lipotoxicity. Few previous studies have reported a causal relationship between FFAs and osteoarthritis pathogenesis. However, molecular mechanism by exert lipotoxicity induce remains largely unknown. We here observed that oleate at usual clinical range does not while high pathological ranges exerted through apoptosis in articular chondrocytes. By investigating differential effect of toxic nontoxic concentrations, we revealed lipid droplet (LD) accumulation confers chondrocytes, resistance to Using fat diet-induced models chondrocytes treated alone or plus palmitate, demonstrated gain protein kinase casein 2 (PKCK2)-six-transmembrane prostate (STAMP2)-and fat-specific 27 (FSP27)-mediated LD accumulation. further exertion FFAs-induced was correlated increased concentration cellular freed from LDs, whether saturated not. In conclusion, PKCK2/STAMP2/FSP27-mediated sequestration rescues osteoarthritic PKCK2/STAMP2/FSP27 should be for interventions against OA.