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首页> 外文期刊>Cytology and genetics >Chitinase 3-like Protein 2 (CHI3L2, YKL-39) Activates Phosphorylation of Extracellular Signal-Regulated Kinases ERK1/ERK2 in Human Embryonic Kidney (HEK293) and Human Glioblastoma (U87 MG) Cells1
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Chitinase 3-like Protein 2 (CHI3L2, YKL-39) Activates Phosphorylation of Extracellular Signal-Regulated Kinases ERK1/ERK2 in Human Embryonic Kidney (HEK293) and Human Glioblastoma (U87 MG) Cells1

机译：几丁质酶3样蛋白2（CHI3L2，YKL-39）激活人胚肾（HEK293）和人胶质母细胞瘤（U87 MG）细胞中细胞外信号调节激酶ERK1 / ERK2的磷酸化1

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Human cartilage chitinase 3-like protein 2 (CHI3L2, YKL-39) is secreted by articular chondro-cytes, also synoviocytes, lung, and heart. Increased levels of YKL-39 have been demonstrated in synovial fluids of patients with rheumatoid or osteoarthritis as well as in some other pathologies and in malignant tumors, particularly in glioblastomas. It belongs to glycosyl hydrolase family 18 and the most closely related to human cartilage glycoprotein 39 (HC gp-39 or chitinase 3-like protein 1, CHI3L1 or YKL-40), which as it was shown previously, promotes the growth of human synovial cells as well as skin and fetal lung fibroblasts. Dose-dependent growth stimulation was observed when the fibroblastic cell line was exposed to YKL-40 in a concentration range from 0.1 to 2 nM, which is similar to the effective dose of the well characterized mitogen, insulin-like growth factor I. The use of selective inhibitors of the mitogen-activated protein kinase (MAP kinase) signaling pathway indicates that both, YKL-40 and IGF-I are involved in phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/ERK2). Thus YKL-40 initiates a signaling cascade which leads to increased cell proliferation, suggesting that this protein could play some role in the inhibition of apoptosis. We report here that YKL-39, which as YKL-40 has significantly increased expression in glioblastomas, also activates signal-regulated kinases ERK1/ERK2 in human embryonic kidney (HEK293) and human glioblastoma (U87 MG) cells.
机译：人软骨几丁质酶3样蛋白2（CHI3L2，YKL-39）由关节软骨细胞，滑膜细胞，肺和心脏分泌。在类风湿性关节炎或骨关节炎患者的滑液中，以及在某些其他病理学和恶性肿瘤中，特别是在成胶质细胞瘤中，已证实YKL-39水平升高。它属于糖基水解酶家族18，与人软骨糖蛋白39（HC gp-39或几丁质酶3样蛋白1，CHI3L1或YKL-40）关系最密切，如前所述，它促进人滑膜的生长。细胞以及皮肤和胎儿的肺成纤维细胞。当成纤维细胞细胞系暴露于浓度范围为0.1至2 nM的YKL-40时，观察到剂量依赖性生长刺激，这与特征明确的促细胞分裂剂胰岛素样生长因子I的有效剂量相似。丝裂原活化蛋白激酶（MAP激酶）信号通路选择性抑制剂的研究表明，YKL-40和IGF-1均参与细胞外信号调节激酶1和2（ERK1 / ERK2）的磷酸化。因此，YKL-40启动信号传导级联反应，导致细胞增殖增加，表明该蛋白可能在抑制细胞凋亡中起作用。我们在这里报告，YKL-39（作为YKL-40在胶质母细胞瘤中的表达显着增加）还激活了人胚胎肾（HEK293）和人胶质母细胞瘤（U87 MG）细胞中的信号调节激酶ERK1 / ERK2。

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    《Cytology and genetics》 |2010年第1期|P.1-6|共6页
  • 作者

    P. A. Areshkov; V. M. Kavsan;

  • 作者单位

    Institute of Molecular Biology and Genetics, 150 Zabolotnogo str., Kyiv, 03680 Ukraine;

    rnInstitute of Molecular Biology and Genetics, 150 Zabolotnogo str., Kyiv, 03680 Ukraine;

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