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首页> 外文期刊>Journal of dermatological science >Human catestatin enhances migration and proliferation of normal human epidermal keratinocytes.
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Human catestatin enhances migration and proliferation of normal human epidermal keratinocytes.

机译：人catestatin增强正常人表皮角质形成细胞的迁移和增殖。

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BACKGROUND: Skin-derived antimicrobial peptides, such as human beta-defensins and cathelicidins, actively contribute to host defense by inactivating microorganisms. Catestatin, a neuroendocrine peptide that affects human autonomic functions, has recently been detected in keratinocytes upon injury/infection where it inhibits the growth of pathogens. Human catestatin exhibits three single nucleotide polymorphisms: Gly364Ser, Pro370Leu, and Arg374Gln. OBJECTIVE: To investigate the effects of human catestatin and its variants on keratinocyte migration and proliferation, and to elucidate the possible signaling mechanisms involved. METHODS: The migration of normal human keratinocytes was analyzed using Boyden microchamber assay and in vitro wound closure assay. Cell proliferation was evaluated by BrdU incorporation, cell count assay and cell cycle analysis. Intracellular Ca(2+) mobilization was measured using a fluorescent calcium assay kit. The phosphorylation of epidermal growth factor receptor (EGFR), Akt, and MAPKs was determined by Western blotting. RESULTS: Catestatin and its variants dose-dependently enhanced keratinocyte migration and proliferation. Moreover, catestatin peptides increased intracellular Ca(2+) mobilization and induced the phosphorylation of EGFR, Akt, extracellular signal-regulated kinase (ERK), and p38 in keratinocytes. The induction of keratinocyte migration and proliferation by catestatin peptides involved G-proteins, phospholipase C, EGFR, PI3-kinase, ERK, and p38, as evidenced by the specific inhibitory effects of pertussis toxin (G-protein inhibitor), U-73122 (phospholipase C inhibitor), AG1478 (EGFR inhibitor), anti-EGFR antibody, wortmannin (PI3-kinase inhibitor), U0126 (ERK inhibitor), and SB203580 (p38 inhibitor), respectively. CONCLUSION: Besides inhibiting the growth of skin pathogens, catestatin peptides may also contribute to cutaneous wound closure by enhancing keratinocyte migration and proliferation at the wound site.
机译：背景：皮肤衍生的抗菌肽，例如人β-防御素和cathelicidin，通过灭活微生物积极地促进宿主防御。 Catestatin是一种影响人类自主功能的神经内分泌肽，最近在损伤/感染后在角质形成细胞中被检测到，它抑制了病原体的生长。人catestatin具有三个单核苷酸多态性：Gly364Ser，Pro370Leu和Arg374Gln。目的：研究人catestatin及其变体对角质形成细胞迁移和增殖的影响，并阐明可能涉及的信号传导机制。方法：采用Boyden微腔室法和体外伤口闭合法分析正常人角质形成细胞的迁移。通过BrdU掺入，细胞计数测定和细胞周期分析评估细胞增殖。使用荧光钙测定试剂盒测量细胞内Ca（2+）动员。通过蛋白质印迹法测定表皮生长因子受体（EGFR），Akt和MAPKs的磷酸化。结果：Catestatin及其变体剂量依赖性地增强了角质形成细胞的迁移和增殖。此外，catestatin肽增加细胞内Ca（2+）的动员并诱导角质形成细胞中EGFR，Akt，细胞外信号调节激酶（ERK）和p38的磷酸化。酪蛋白肽诱导的角质形成细胞迁移和增殖涉及G蛋白，磷脂酶C，EGFR，PI3-激酶，ERK和p38，如百日咳毒素（G蛋白抑制剂），U-73122（磷脂酶C抑制剂），AG1478（EGFR抑制剂），抗EGFR抗体，渥曼青霉素（PI3-激酶抑制剂），U0126（ERK抑制剂）和SB203580（p38抑制剂）。结论：除了抑制皮肤病原体的生长外，他汀类肽还可以通过促进伤口处角质形成细胞的迁移和增殖来促进皮肤伤口的闭合。

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