Keratinocyte derived extracellular vesicles mediated crosstalk between epidermis and dermis in UVB-induced skin inflammation.

IF 8.2 2区生物学 Q1 CELL BIOLOGY

Cell Communication and Signaling Pub Date : 2024-09-30 DOI:10.1186/s12964-024-01839-9

Yubin Li, Avital Baniel, DeAnna Diaz, Mariko Ogawa-Momohara, Cristina Ricco, Ahmed Eldaboush, Muhammad Bashir, Meena Sharma, Ming-Lin Liu, Victoria P Werth

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Abstract

Background and rationale: Ultraviolet-B (UVB) light induces dermal inflammation, although it is mostly absorbed in the epidermis. Recent reports suggest extracellular vesicles (EVs) act as a mediator of photodamage signaling. Melatonin is reported to be a protective factor against UV-induced damage. We hypothesized that EVs derived from UVB-irradiated keratinocytes might trigger proinflammatory responses in dermal cells and tested whether melatonin can ameliorate UVB-induced inflammation.

Methods: We used UVB-irradiated HaCaT cells, primary keratinocytes and STING knock-out mice to model production of EVs under photodamaging conditions and performed immunoblotting and ELISA to measure their effect on dermal macrophages.

Results: UVB-irradiated keratinocytes produce an increased number of EVs that contain higher concentrations of DNA and protein compared with controls. KC-derived EVs (KEVs) induced a STING- and inflammasome-mediated proinflammatory response in macrophages in vitro, and a pronounced inflammatory infiltrate in mouse dermis in vivo. Melatonin ameliorated KEVs inflammatory effect both in vitro and in vivo.

Conclusions: This data suggests EVs are mediators in a crosstalk that takes place between keratinocytes and their neighboring cells as a result of photodamage. Further studies exploring EVs induced by damaging doses of UVB, and their impact on other cells will provide insight into photodamage and may help develop targeted therapeutic approaches.

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角质细胞衍生的细胞外囊泡在紫外线诱导的皮肤炎症中介导了表皮和真皮之间的串联。

背景和原理：紫外线-B（UVB）光可诱发真皮炎症，尽管它主要被表皮吸收。最近的报告表明，细胞外囊泡（EVs）是光损伤信号传导的介质。据报道，褪黑素是防止紫外线引起的损伤的保护因子。我们推测，从经 UVB 照射的角朊细胞中提取的 EVs 可能会引发真皮细胞的促炎反应，并测试了褪黑激素是否能改善 UVB 诱导的炎症：我们使用经 UVB 照射的 HaCaT 细胞、原代角朊细胞和 STING 基因敲除小鼠来模拟光损伤条件下 EVs 的产生，并进行免疫印迹和 ELISA 检测其对真皮巨噬细胞的影响：结果：与对照组相比，经 UVB 照射的角质形成细胞产生的 EVs 数量增加，其中 DNA 和蛋白质的含量更高。KC 衍生的 EVs（KEVs）在体外诱导巨噬细胞产生 STING 和炎症体介导的促炎反应，在体内诱导小鼠真皮层出现明显的炎症浸润。褪黑素可改善 KEVs 在体外和体内的炎症效应：这些数据表明，EVs 是光损伤导致的角朊细胞及其邻近细胞之间串联的介质。进一步研究探索破坏性剂量 UVB 诱导的 EVs 及其对其他细胞的影响将有助于深入了解光损伤，并有助于开发有针对性的治疗方法。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Communication and Signaling CELL BIOLOGY-

CiteScore

11.00

自引率

0.00%

发文量

180

期刊介绍： Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.