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划痕诱导的部分皮肤伤口通过独立迁移的角蛋白细胞片再上皮化。

Scratch-induced partial skin wounds re-epithelialize by sheets of independently migrating keratinocytes.

机构信息

Division of Molecular Pathology, Oncode Institute, Netherlands Cancer Institute, Amsterdam, The Netherlands.

Institute of Molecular and Cellular Anatomy, Rheinisch-Westfälische Technische Hochschule Aachen University, Aachen, Germany.

出版信息

Life Sci Alliance. 2020 Nov 30;4(1). doi: 10.26508/lsa.202000765. Print 2021 Jan.

DOI:10.26508/lsa.202000765
PMID:33257474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7723264/
Abstract

Re-epithelialization is a crucial process to reestablish the protective barrier upon wounding of the skin. Although this process is well described for wounds where the complete epidermis and dermis is damaged, little is known about the re-epithelialization strategy in more frequently occurring smaller scratch wounds in which structures such as the hair follicles and sweat glands stay intact. To study this, we established a scratch wound model to follow individual keratinocytes in all epidermal layers in the back skin of mice by intravital microscopy. We discover that keratinocytes adopt a re-epithelialization strategy that enables them to bypass immobile obstacles such as hair follicles. Wound-induced cell loss is replenished by proliferation in a distinct zone away from the wound and this proliferation does not affect overall migration pattern. Whereas suprabasal keratinocytes are rather passive, basal keratinocytes move as a sheet of independently migrating cells into the wound, thereby constantly changing their direct neighboring cells enabling them to bypass intact obstacles. This re-epithelialization strategy results in a fast re-establishment of the protective skin barrier upon wounding.

摘要

上皮化是皮肤创伤后重建保护屏障的关键过程。尽管这个过程在完整的表皮和真皮受损的伤口中得到了很好的描述,但对于更常见的较小划痕伤口中,上皮化策略知之甚少,这些伤口中的结构如毛囊和汗腺仍然完整。为了研究这一点,我们通过活体显微镜建立了一个划痕伤口模型,以跟踪小鼠背部皮肤所有表皮层中的单个角质形成细胞。我们发现,角质形成细胞采用了一种上皮化策略,使它们能够绕过毛囊等固定不动的障碍物。通过在远离伤口的特定区域增殖来补充诱导性细胞丢失,而这种增殖不会影响整体迁移模式。虽然上层角质形成细胞比较被动,但基底角质形成细胞作为一层独立迁移的细胞进入伤口移动,从而不断改变它们的直接相邻细胞,使它们能够绕过完整的障碍物。这种上皮化策略导致伤口后快速重建保护性皮肤屏障。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/360422ef5deb/LSA-2020-00765_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/4d421606585e/LSA-2020-00765_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/c6dcf1d976ed/LSA-2020-00765_FigS1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/2bbcdf2a87f9/LSA-2020-00765_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/b10575a13fdb/LSA-2020-00765_FigS3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/360422ef5deb/LSA-2020-00765_Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/4d421606585e/LSA-2020-00765_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/c6dcf1d976ed/LSA-2020-00765_FigS1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/2bbcdf2a87f9/LSA-2020-00765_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/b10575a13fdb/LSA-2020-00765_FigS3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bef7/7723264/360422ef5deb/LSA-2020-00765_Fig4.jpg

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