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创伤性脑损伤可诱导切口皮肤伤口产生早期屏障保护反应,加速皮肤伤口愈合。

Traumatic Brain Injury Induces Early Barrier Protective Responses in Incisional Skin Wounds Accelerating Cutaneous Wound Healing.

作者信息

Aghapour Mahyar, Heuvel Florian Olde, Fröhlich Albrecht, Heinzl Adelheid, Maity Pallab, Singh Karmveer, Wang Yongfang, Cheng Jinnan, Roselli Francesco, Scharffetter-Kochanek Karin

机构信息

Department of Dermatology and Allergic Diseases, Ulm University, Ulm, Germany.

Department of Neurology, Ulm University, Ulm, Germany.

出版信息

Wound Repair Regen. 2025 Sep-Oct;33(5):e70079. doi: 10.1111/wrr.70079.

DOI:10.1111/wrr.70079
PMID:40879095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12395893/
Abstract

Though Traumatic Brain Injury (TBI) and skin trauma often occur together, it is unresolved whether TBI changes the healing of skin wounds. We here explored whether TBI impacts the sequence of events during skin wound healing. Incisional skin wounds from mice subjected to TBI were assessed employing unbiased transcriptome analysis and immunostaining. Transcriptome analysis at day 1 after combined trauma detects a significant enrichment of genes involved in macrophage and T cell recruitment and activation in contrast to skin wounds without TBI. At day 7 after combined trauma, genes in pathways of re-epithelialisation including cornification and keratinisation and of anti-inflammatory responses were highly enriched. These findings were confirmed by immunostaining with increased re-epithelialisation and cornification and an increased number of macrophages and T cells resolving inflammation. Moreover, the number of dermal myofibroblasts is highly increased in skin wounds after combined trauma. Collectively, TBI induces a robust defence response characterised by early onset of enhanced immunity, faster epidermal barrier formation, and myofibroblast-driven acceleration of wound closure, which may together help counteract systemic infection.

摘要

尽管创伤性脑损伤(TBI)和皮肤创伤常同时发生,但TBI是否会改变皮肤伤口的愈合情况仍未得到解决。我们在此探究了TBI是否会影响皮肤伤口愈合过程中的一系列事件。通过无偏转录组分析和免疫染色对遭受TBI的小鼠的切口皮肤伤口进行了评估。与未发生TBI的皮肤伤口相比,联合创伤后第1天的转录组分析检测到参与巨噬细胞和T细胞募集及激活的基因显著富集。联合创伤后第7天,包括角质化和角化在内的再上皮化途径以及抗炎反应途径中的基因高度富集。这些发现通过免疫染色得到证实,再上皮化和角化增加,解决炎症的巨噬细胞和T细胞数量增加。此外,联合创伤后皮肤伤口中的真皮肌成纤维细胞数量大幅增加。总体而言,TBI会引发强大的防御反应,其特征为免疫力增强的早期发作、更快的表皮屏障形成以及肌成纤维细胞驱动的伤口闭合加速,这些可能共同有助于抵御全身感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/8a73545ab66a/WRR-33-0-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/48ac5fe95f94/WRR-33-0-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/5862e3293ea4/WRR-33-0-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/cd1f08be7211/WRR-33-0-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/8a73545ab66a/WRR-33-0-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/48ac5fe95f94/WRR-33-0-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/5862e3293ea4/WRR-33-0-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/cd1f08be7211/WRR-33-0-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d053/12395893/8a73545ab66a/WRR-33-0-g003.jpg

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本文引用的文献

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Local administration of regulatory T cells promotes tissue healing.局部给予调节性 T 细胞可促进组织愈合。
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MDK promotes M2 macrophage polarization to remodel the tumour microenvironment in clear cell renal cell carcinoma.MDK 促进 M2 巨噬细胞极化以重塑肾透明细胞癌的肿瘤微环境。
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A single-cell atlas deconstructs heterogeneity across multiple models in murine traumatic brain injury and identifies novel cell-specific targets.
单细胞图谱解析了小鼠创伤性脑损伤中多个模型的异质性,并确定了新的细胞特异性靶点。
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IGF-1 inhibits inflammation and accelerates angiogenesis via Ras/PI3K/IKK/NF-κB signaling pathways to promote wound healing.IGF-1 通过 Ras/PI3K/IKK/NF-κB 信号通路抑制炎症反应并促进血管生成,从而促进伤口愈合。
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Traumatic brain injury stimulates sympathetic tone-mediated bone marrow myelopoiesis to favor fracture healing.创伤性脑损伤刺激交感神经介导的骨髓髓系细胞生成,有利于骨折愈合。
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The meningeal transcriptional response to traumatic brain injury and aging.脑膜对创伤性脑损伤和衰老的转录反应。
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