Effect of growth factors on antimicrobial peptides and pro-inflammatory mediators during wound healing
Effect of growth factors on antimicrobial peptides and pro-inflammatory mediators during wound healing
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DOI：
10.1007/s00784-014-1239-9
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发表时间：
2015-03-01
影响因子：
3.4
通讯作者：
Jepsen, S.
中科院分区：
文献类型：
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作者：
Dommisch, H.;Winter, J.;Jepsen, S.
抗菌肽 (AMP)，例如人 β-防御素-2 (hBD-2) 和 CC-趋化因子配体 20 (CCL20)，表现出直接的杀菌作用和类似介质的活性。据推测，受伤会诱导 AMP 和促炎介质的表达，而内源性介质，例如胰岛素样生长因子-1 (IGF-1) 和转化生长因子-α (TGF-α)，会调节这种诱导的表达。 来自三个不同供体的单层牙龈上皮细胞 (GEC) 和牙龈成纤维细胞 (HGF) 受伤 在 IGF-1 和 TGF-α 存在（测试组）或不存在（对照组）的情况下使用划痕试验（体外创伤）。随着时间的推移（0、6、24、48、72 小时）监测体外伤口闭合，并对伤口区域进行显微镜分析（Axio-VisionA 软件，Zeiss）。通过 qPCR 对 GAPDH、hBD-2、CCL20、白细胞介素 1 β (IL-1 β) 和白细胞介素 8 (IL-8) 进行基因表达分析。与对照细胞相比，IGF-1 和 TGF-α 显着增强体外伤口闭合（P < 0.05）。在 GEC 中，与对照细胞相比，IGF-1 诱导 IL-1β 和 IL-8 的基因表达（P < 0.05）。在 HGF 中，损伤本身诱导了 hBD-2、CCL20 和 IL-1 beta 的信使 RNA，而 IGF-1 和 TGF-α 则逆转了这种效应（P < 0.05）。在牙龈细胞中，AMP 的基因表达因损伤而改变，内源性生长因子进一步影响了表达谱，但个体间差异较大。
Antimicrobial peptides (AMPs), such as human beta-defensin-2 (hBD-2) and the CC-chemokine ligand 20 (CCL20), exhibit direct microbicidal effects and mediator-like activity. It was hypothesized that wounding induces the expression of AMPs and pro-inflammatory mediators and that endogenous mediators, such as insulin-like growth factor-1 (IGF-1) and transforming growth factor-alpha (TGF-alpha), modulate this induced expression.Monolayers of gingival epithelial cells (GECs) and gingival fibroblast (HGFs) from three different donors were wounded using the scratch assay (in vitro wounding) in the presence (test group) or absence (control group) of IGF-1 and TGF-alpha. In vitro wound closure was monitored over time (0, 6, 24, 48, 72 h), and wound areas were microscopically analyzed (Axio-VisionA (R) Software, Zeiss). Gene expression analysis of the GAPDH, hBD-2, CCL20, interleukin-1 beta (IL-1 beta), and interleukin-8 (IL-8) was performed by qPCR.In comparison to control cells, IGF-1 and TGF-alpha significantly enhanced in vitro wound closure (P < 0.05). In GECs, IGF-1 induced the gene expression of IL-1 beta and IL-8 when compared to control cells (P < 0.05). In HGFs, wounding per se induced the messenger RNA of hBD-2, CCL20, and IL-1 beta, whereas IGF-1 and TGF-alpha reversed this effect (P < 0.05).In gingival cells, the gene expression of AMPs was altered by injury, and endogenous growth factors further influenced the expression profiles, but with high interindividual differences.