Human gingival fibroblasts express functional chemokine receptor CXCR6
Human gingival fibroblasts express functional chemokine receptor CXCR6
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DOI：
10.1111/j.1365-2249.2009.03915.x
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发表时间：
2009-06-01
影响因子：
4.6
通讯作者：
Matsuo, T.
中科院分区：
文献类型：
--
作者：
Hosokawa, Y.;Hosokawa, I.;Matsuo, T.
我们已经报道了新近发现的跨膜趋化因子CXCL16在人牙龈成纤维细胞(HGF)中表达。然而，目前尚不清楚HGF表达CXCL16的受体CXCR6，还是CXCL16影响HGF的生物学。逆转录-聚合酶链式反应和流式细胞仪分析表明，HGF表达CXCR6。此外，我们还阐明了肿瘤坏死因子α和胞嘧啶鸟嘌呤二核苷酸(CpG)DNA(Toll样受体9配体)对HGF诱导的CXCR6表达的促进作用。IL-4、IL-13和CpG DNA通过肿瘤坏死因子-α刺激HGF上调CXCR6的表达。另一方面，IL-1β和干扰素-γ抑制肿瘤坏死因子-α处理的HGF上CXCR6的表达。CXCL16可诱导HGF增殖和细胞外调节蛋白激酶(ERK)和蛋白激酶B(AKT)的磷酸化。综上所述，由于CXCL16诱导HGF增殖和ERK、AKT磷酸化，HGF在功能上表达CXCR6。这些结果表明，CXCL16可能在牙周病组织的发生和重塑中起重要作用。
We have reported that CXCL16, a recently discovered transmembrane chemokine, is expressed in human gingival fibroblasts (HGF). However, it is not known whether HGF express CXCR6, the receptor for CXCL16, or CXCL16 affects HGF biology. We have shown that HGF expressed CXCR6 by reverse transcription-polymerase chain reaction and flow cytometric analysis. Moreover, we elucidated that tumour necrosis factor (TNF)-alpha and cytosine-guanine dinucleotide (CpG) DNA (Toll-like receptor-9 ligand) treatment enhanced CXCR6 expression by HGF. Interleukin (IL)-4, IL-13 and CpG DNA up-regulated CXCR6 expression by TNF-alpha-stimulated HGF. On the other hand, IL-1 beta and interferon-gamma inhibited CXCR6 expression on TNF-alpha-treated HGF. CXCL16 treatment induced HGF proliferation and phosphorylation of extracellular regulated kinase (ERK) and protein kinase B (AKT) in HGF. In conclusion, HGF expressed CXCR6 functionally, because CXCL16 induced HGF proliferation and ERK and AKT phosphorylation in HGF. These results indicate that CXCL16 may play an important role in the pathogenesis and remodelling in periodontally diseased tissues.