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SNORC knockdown alleviates inflammation, autophagy defect and matrix degradation of chondrocytes in osteoarthritis development

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Abstract

Excessive inflammation and autophagy defect of chondrocytes play important roles in the pathological process of osteoarthritis (OA). The present study aimed to clarify the roles of small novel rich in cartilage (SNORC) in these pathological changes of chondrocytes in OA. Bioinformatics analysis of GEO dataset GSE207881 displayed that SNORC was a potential biomarker for OA. As confirmed by quantitative real-time PCR, immunohistochemical staining and western blotting, SNORC was significantly up-regulated in cartilage of OA rat model and interleukin (IL)-1β-stimulated primary rat articular chondrocytes in contrast to their corresponding normal control. Knocking down SNORC in IL-1β-induced chondrocytes obviously suppressed the production of nitric oxide (NO), IL-6, tumor necrosis factor (TNF)-α and prostaglandin E2 (PGE2) to alleviate inflammation, and reduced the protein levels of a disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5) and matrix metallopeptidase (MMP)13 and elevated collagen type 2 alpha 1 (COL2A1) level to improve matrix degradation. Down-regulation of SNORC increased Beclin1 expression and LC3II/LC3I ratio, but suppressed p62 expression to restore impaired autophagy in IL-1β-induced chondrocytes. Moreover, down-regulating SNORC mitigated mitochondrial dysfunction and apoptosis in IL-1β-stimulated chondrocytes. Mechanically, SNORC simultaneously activated the phosphatidylinositol-3-kinase/serine threonine kinase (PI3K/AKT) and c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway in the IL-1β-induced chondrocyte, while re-activating the PI3K and JNK signals abolished the suppressive effect of down-regulating SNORC on IL-1β-induced chondrocyte damage. In a word, SNORC knockdown alleviates inflammation, matrix degradation, autophagy defect and excessive apoptosis of chondrocytes during OA development via suppressing the PI3K and JNK signaling pathway.

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The data were all included in this paper. The original data are available from the corresponding author upon reasonable request.

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Funding

This research was supported by the Yunnan Traumatology and Orthopedics Clinical Medical Center (Grant No. ZX20191001), the Grants from Yunnan Orthopedics and Sports Rehabilitation Clinical Medicine Research Center (Grant No. 202102AA310068) and Technical Innovation Talents Training Object Project (Grant No. 202005AD160146).

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Authors and Affiliations

  1. Clinical Medical College of Dali University, Dali, 671000, China

    Zhifang Tang & Hanzhen Feng

  2. Kunming Medical University, Kunming, 650500, China

    Xusheng Chen

  3. Yunnan University of Chinese Medicine, Kunming, 650500, China

    Shuiyan Shao

  4. Institute of Traumatology and Orthopedics, 920th Hospital of Joint Logistics Support Force, PLA, No.212 Daguan Road, Xishan District, Kunming, Yunnan, 650000, China

    Chuan Li

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Conceptualization: Zhifang Tang, Chuan Li; Methodology: Zhifang Tang, Hanzhen Feng; Investigation: Hanzhen Feng, Xusheng Chen; Visualization: Shuiyan Shao; Writing - original draft preparation: Zhifang Tang; Writing - revising: Xusheng Chen, Shuiyan Shao; Funding acquisition: Chuan Li; Supervision: Chuan Li. All authors read and approved the final manuscript.

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The experiment protocol involving in animals was approved by the ethics committee of 920th Hospital of Joint Logistics Support Force, PLA. All the operations involved in animals followed the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals and ARRIVE Guidelines pertaining to animal experimentation.

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Tang, Z., Feng, H., Chen, X. et al. SNORC knockdown alleviates inflammation, autophagy defect and matrix degradation of chondrocytes in osteoarthritis development. Mol Cell Biochem (2023). https://doi.org/10.1007/s11010-023-04842-9

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