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SPRR1B+ 角质形成细胞通过激活 STAT3 为口腔黏膜的快速愈合做好准备。

SPRR1B+ keratinocytes prime oral mucosa for rapid wound healing via STAT3 activation.

机构信息

Department of Dermatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

Shanghai Institute of Precision Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

出版信息

Commun Biol. 2024 Sep 16;7(1):1155. doi: 10.1038/s42003-024-06864-5.

DOI:10.1038/s42003-024-06864-5
PMID:39300285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11413210/
Abstract

Oral mucosal wounds exhibit accelerated healing with reduced scarring compared to cutaneous wounds, representing an optimal wound healing paradigm. However, the specific cellular subtypes orchestrating the efficient healing of mucosal tissues remain elusive. Through a comprehensive analysis integrating bulk-mRNA and single-cell sequencing data during the wound healing process in oral mucosa and skin, we have delineated a distinct set of genes markedly upregulated during tissue repair. This collection of wound healing-associated genesets was highly enriched in a specific keratinocyte subpopulation identified as STAT3-activated SPRR1B+ keratinocytes. Notably, despite the inherent rapidity of oral mucosal healing, the induction of SPRR1B+ keratinocytes is evident in both skin and mucosal wound healing processes in murine model. Intriguingly, these wound healing-promoting SPRR1B+ keratinocytes, which are induced via STAT3 activation, inherently abundant in unwounded normal mucosa but absent in normal skin. SPRR1B knockdown significantly inhibits mucosal keratinocyte migration, a critical attribute for effective wound healing. In summary, through analysis of human oral and skin wound healing processes at single-cell resolution, coupled with validation in murine model, suggests STAT3-activated SPRR1B+ keratinocytes are associated with the rapid mucosal repair process. This discovery underscores the potential application of SPRR1B+ keratinocytes in the therapeutic management of chronic or non-healing wounds.

摘要

口腔黏膜伤口的愈合速度比皮肤伤口快，且疤痕形成较少，代表了一种理想的伤口愈合模式。然而，调控黏膜组织高效愈合的确切细胞亚型仍不清楚。通过整合口腔黏膜和皮肤伤口愈合过程中的 bulk-mRNA 和单细胞测序数据的全面分析，我们描绘了一组在组织修复过程中明显上调的特定基因。这些与伤口愈合相关的基因集在一个特定的角蛋白细胞亚群中高度富集，该亚群被鉴定为 STAT3 激活的 SPRR1B+角蛋白细胞。值得注意的是，尽管口腔黏膜的愈合速度很快，但在皮肤和黏膜伤口愈合过程中，小鼠模型中均能诱导 SPRR1B+角蛋白细胞。有趣的是，这些通过 STAT3 激活诱导的促进伤口愈合的 SPRR1B+角蛋白细胞在未受伤的正常黏膜中固有丰富，但在正常皮肤中不存在。SPRR1B 敲低显著抑制了黏膜角质形成细胞的迁移，这是有效伤口愈合的关键属性。总之，通过单细胞分辨率分析人类口腔和皮肤伤口愈合过程，并在小鼠模型中进行验证，表明 STAT3 激活的 SPRR1B+角蛋白细胞与快速的黏膜修复过程有关。这一发现强调了 SPRR1B+角蛋白细胞在慢性或非愈合性伤口的治疗管理中的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/3ba451ff43fa/42003_2024_6864_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/95a4e4d144ca/42003_2024_6864_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/8c242a008b98/42003_2024_6864_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/6a8d74ed996a/42003_2024_6864_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/d9b7094b02de/42003_2024_6864_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/8979db2b6012/42003_2024_6864_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/593fcf85ea95/42003_2024_6864_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/4ad13e4404f9/42003_2024_6864_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/3ba451ff43fa/42003_2024_6864_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/95a4e4d144ca/42003_2024_6864_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/8c242a008b98/42003_2024_6864_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/6a8d74ed996a/42003_2024_6864_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/d9b7094b02de/42003_2024_6864_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/8979db2b6012/42003_2024_6864_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/593fcf85ea95/42003_2024_6864_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/4ad13e4404f9/42003_2024_6864_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de6/11413210/3ba451ff43fa/42003_2024_6864_Fig8_HTML.jpg

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