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转化生长因子-β1 增加白细胞介素 4 刺激的人牙周韧带细胞中 C-C 趋化因子配体 11 的产生。

Transforming growth factor-β1 increases C-C chemokine ligand 11 production in interleukin 4-stimulated human periodontal ligament cells.

机构信息

Department of Conservative Dentistry, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.

Department of Oral Health Care Promotion, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.

出版信息

Cell Biol Int. 2018 Sep;42(10):1395-1400. doi: 10.1002/cbin.11030. Epub 2018 Jul 24.

Abstract

Transforming growth factor (TGF)-β1 is a multifunctional cytokine, which can control certain functions of various kinds of cells. However, it is unclear whether TGF-β1 affects T-cell migration in periodontal lesions. The aim of this study was to examine the effects of TGF-β1 on the production of C-C chemokine ligand (CCL)11, which is a T-helper 2-type chemokine, in human periodontal ligament cells (HPDLC). Interleukin (IL)-4 induced CCL11 production, but TGF-β1 did not, in HPDLC. However, TGF-β1 enhanced CCL11 production in IL-4-stimulated HPDLC. Western blot analysis showed that the signal transducer and activator of transcription 6 (STAT6) pathway was highly activated in HPDLC that had been stimulated with both IL-4 and TGF-β1. Mitogen-activated protein kinase activation did not differ between the HPDLC treated with a combination of IL-4 and TGF-β1 and those treated with IL-4 or TGF-β1 alone. Moreover, a STAT6 inhibitor significantly inhibited CCL11 production in HPDLC that had been stimulated with IL-4 and TGF-β1. The current study clearly demonstrated that TGF-β1 enhanced IL-4-induced CCL11 production in HPDLC. The STAT6 pathway is important for CCL11 production in IL-4- and TGF-β1-treated HPDLC.

摘要

转化生长因子 (TGF)-β1 是一种多功能细胞因子,可控制各种细胞的某些功能。然而,TGF-β1 是否影响牙周病变中的 T 细胞迁移尚不清楚。本研究旨在研究 TGF-β1 对人牙周韧带细胞 (HPDLC) 中 T 辅助 2 型趋化因子 C-C 趋化因子配体 (CCL)11 产生的影响。白细胞介素 (IL)-4 诱导 CCL11 的产生,但 TGF-β1 没有,在 HPDLC。然而,TGF-β1 增强了 IL-4 刺激的 HPDLC 中 CCL11 的产生。Western blot 分析表明,IL-4 和 TGF-β1 刺激的 HPDLC 中信号转导和转录激活因子 6 (STAT6) 途径高度激活。与单独用 IL-4 或 TGF-β1 处理的 HPDLC 相比,用 IL-4 和 TGF-β1 处理的 HPDLC 中的丝裂原活化蛋白激酶激活没有差异。此外,STAT6 抑制剂显著抑制了 IL-4 和 TGF-β1 刺激的 HPDLC 中 CCL11 的产生。本研究清楚地表明,TGF-β1 增强了 IL-4 诱导的 HPDLC 中 CCL11 的产生。STAT6 途径对于 IL-4 和 TGF-β1 处理的 HPDLC 中 CCL11 的产生很重要。

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