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阐明角蛋白细胞衍生细胞外囊泡对皮肤归巢细胞的作用。

Shedding light on the role of keratinocyte-derived extracellular vesicles on skin-homing cells.

机构信息

Department of Tissue Engineering and Cell Therapy, School of Advanced Technologies in Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.

Transplant Research Center, Shiraz University of Medical Sciences, Khalili Street, Shiraz, 7193711351, Iran.

出版信息

Stem Cell Res Ther. 2020 Sep 29;11(1):421. doi: 10.1186/s13287-020-01929-8.

DOI:10.1186/s13287-020-01929-8
PMID:32993791
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7523352/
Abstract

Extracellular vesicles (EVs) are secretory lipid membranes with the ability to regulate cellular functions by exchanging biological components between different cells. Resident skin cells such as keratinocytes, fibroblasts, melanocytes, and inflammatory cells can secrete different types of EVs depending on their biological state. These vesicles can influence the physiological properties and pathological processes of skin, such as pigmentation, cutaneous immunity, and wound healing. Since keratinocytes constitute the majority of skin cells, secreted EVs from these cells may alter the pathophysiological behavior of other skin cells. This paper reviews the contents of keratinocyte-derived EVs and their impact on fibroblasts, melanocytes, and immune cells to provide an insight for better understanding of the pathophysiological mechanisms of skin disorders and their use in related therapeutic approaches.

摘要

细胞外囊泡 (EVs) 是具有分泌脂质膜的能力,能够通过在不同细胞之间交换生物成分来调节细胞功能。驻留皮肤细胞(如角质形成细胞、成纤维细胞、黑素细胞和炎性细胞)可以根据其生物学状态分泌不同类型的 EVs。这些囊泡可以影响皮肤的生理特性和病理过程,如色素沉着、皮肤免疫和伤口愈合。由于角质形成细胞构成了大部分皮肤细胞,因此这些细胞分泌的 EVs 可能会改变其他皮肤细胞的病理生理行为。本文综述了角质形成细胞衍生的 EVs 的内容及其对成纤维细胞、黑素细胞和免疫细胞的影响,为更好地理解皮肤疾病的病理生理机制及其在相关治疗方法中的应用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9486/7523352/3a43d6653a16/13287_2020_1929_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9486/7523352/3a43d6653a16/13287_2020_1929_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9486/7523352/3a43d6653a16/13287_2020_1929_Fig1_HTML.jpg

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