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Sema4D Aggravated LPS-Induced Injury via Activation of the MAPK Signaling Pathway in ATDC5 Chondrocytes.

Abstract
Osteoarthritis (OA) is the most common chronic degenerative joint disease, and it remains the main cause of chronic disability in elderly individuals. Sema4D (semaphorin 4D) is involved in the immune system and related to bone injury, osteoporosis, osteoblast differentiation, and rheumatoid arthritis. However, the role of Sema4D in OA remains unclear. Hence, the LPS-stimulated chondrocyte cell injury model was constructed in this study to investigate the role of Sema4D in OA development. The results showed that Sema4D was increased in LPS-treated ATDC5 cells, and the knockdown of Sema4D suppressed the decline of cell viability, the increase of cell apoptosis, and the increase of IL-6, IL-1β, and TNF-α secretion in ATDC5 cells induced by LPS. Meanwhile, Sema4D overexpression aggravated the cell injury triggered by LPS, and inhibiting Plexin B1 partly abolished the effect of Sema4D overexpression on LPS-induced chondrocyte injury. Furthermore, silencing of Sema4D blocked the activation of the MAPK pathway in LPS-stimulated ATDC5 cells. Enhanced Sema4D promoted the activation of the MAPK pathway in LPS-stimulated ATDC5 cells. What is more, inhibiting the MAPK signaling pathway abolished the promoting effect of Sema4D overexpression on LPS-induced chondrocyte injury. Therefore, our study suggested that the knockdown of Sema4D protects ATDC5 cells against LPS-induced injury through inactivation of the MAPK signaling pathway via interacting with Plexin B1.
AuthorsJinlai Lei, Yahui Fu, Yan Zhuang, Kun Zhang
JournalBioMed research international (Biomed Res Int) Vol. 2020 Pg. 8691534 ( 2020) ISSN: 2314-6141 [Electronic] United States
PMID32382577 (Publication Type: Journal Article)
CopyrightCopyright © 2020 Jinlai Lei et al.
Chemical References
  • Antigens, CD
  • CD100 antigen
  • Cytokines
  • Lipopolysaccharides
  • Nerve Tissue Proteins
  • PLXNB1 protein, human
  • Receptors, Cell Surface
  • Semaphorins
Topics
  • Antigens, CD (genetics, metabolism)
  • Cell Line
  • Chondrocytes (metabolism, pathology)
  • Cytokines (genetics, metabolism)
  • Humans
  • Lipopolysaccharides (toxicity)
  • MAP Kinase Signaling System (drug effects)
  • Nerve Tissue Proteins (genetics, metabolism)
  • Osteoarthritis (genetics, metabolism, pathology)
  • Receptors, Cell Surface (genetics, metabolism)
  • Semaphorins (genetics, metabolism)

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