• World Neurosurg · Jan 2020

    T140 inhibits apoptosis and promotes proliferation and matrix formation through the SDF-1/CXCR4 signaling pathway in endplate chondrocytes of the rat intervertebral discs.

    • Zhi-Yong Gao, Liang-Liang Yu, Ben-Xia Shi, Zhen-Ling Dong, Yu-Jie Sun, and Hou-Sheng Ma.
    • Department of Rehabilitation, Yantai Yuhuangding Hospital, Yantai, China.
    • World Neurosurg. 2020 Jan 1; 133: e165-e172.

    BackgroundCartilaginous endplate (CEP), a thin layer of hyaline cartilage located between the vertebral endplate and nucleus pulposus, transports the nutrient into the disc. The objective of this study was to evaluate the influence of T140 (polyphemusin II-derived peptide) on the CEP cell growth, apoptosis, and the matrix formation via the stromal cell-derived factor-1 (SDF-1)/cysteine X cysteine (CXC) receptor-4 (CXCR4) signaling pathway.MethodsSprague-Dawley rats were euthanized by cervical dislocation and dissected for the isolation and the appraisal of CEP cells that were extracted from the endplate in rat intervertebral discs and were then added with different concentrations of reagents (SDF-1 and T140). The effect of T140 on CEP cell proliferation and apoptosis were analyzed. The messenger RNA (mRNA) and protein expressions of CXCR4, prominin-1, proteoglycans, type II collagen, B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein were analyzed by reverse transcription quantitative polymerase chain reaction and Western blot analysis.ResultsT140 promoted the proliferation of CEP cells and inhibited the apoptosis of CEP cells. Additionally, T140 suppressed the mRNA and protein expression of CXCR4, prominin-1, and Bcl-2 associated X protein, and increased the mRNA and protein expression of proteoglycans, type II collagen, and Bcl-2.ConclusionsT140 promotes the proliferation and matrix formation and inhibits the apoptosis of CEP cells by blocking the SDF-1/CXCR4 signaling pathway in vitro, which provides a certain therapeutic effect on the degeneration of intervertebral discs.Copyright © 2019 Elsevier Inc. All rights reserved.

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