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肥大细胞在创伤愈合中的作用研究进展:涉及的分子和细胞机制

A Review of the Contribution of Mast Cells in Wound Healing: Involved Molecular and Cellular Mechanisms.

机构信息

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Department of Immunology, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Clin Rev Allergy Immunol. 2020 Jun;58(3):298-312. doi: 10.1007/s12016-019-08729-w.

Abstract

Mast cells (MCs), apart from their classic role in allergy, contribute to a number of biologic processes including wound healing. In particular, two aspects of their histologic distribution within the skin have attracted the attention of researchers to study their wound healing role; they represent up to 8% of the total number of cells within the dermis and their cutaneous versions are localized adjacent to the epidermis and the subdermal vasculature and nerves. At the onset of a cutaneous injury, the accumulation of MCs and release of proinflammatory and immunomodulatory mediators have been well documented. The role of MC-derived mediators has been investigated through the stages of wound healing including inflammation, proliferation, and remodeling. They contribute to hemostasis and clot formation by enhancing the expression of factor XIIIa in dermal dendrocytes through release of TNF-α, and contribute to clot stabilization. Keratinocytes, by secreting stem cell factor (SCF), recruit MCs to the site. MCs in return release inflammatory mediators, including predominantly histamine, VEGF, interleukin (IL)-6, and IL-8, that contribute to increase of endothelial permeability and vasodilation, and facilitate migration of inflammatory cells, mainly monocytes and neutrophils to the site of injury. MCs are capable of activating the fibroblasts and keratinocytes, the predominant cells involved in wound healing. MCs stimulate fibroblast proliferation during the proliferative phase via IL-4, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) to produce a new extracellular matrix (ECM). MC-derived mediators including fibroblast growth factor-2, VEGF, platelet-derived growth factor (PDGF), TGF-β, nerve growth factor (NGF), IL-4, and IL-8 contribute to neoangiogenesis, fibrinogenesis, or reepithelialization during the repair process. MC activation inhibition and targeting the MC-derived mediators are potential therapeutic strategies to improve wound healing through reduced inflammatory responses and scar formation.

摘要

肥大细胞(MCs)除了在过敏中的经典作用外,还参与许多生物学过程,包括伤口愈合。特别是,它们在皮肤中的组织学分布的两个方面引起了研究人员的注意,以研究其伤口愈合作用;它们在真皮中占细胞总数的 8%,并且其皮肤形式位于表皮和皮下血管和神经附近。在皮肤损伤发生时,MC 的积累和促炎和免疫调节介质的释放已得到充分证明。已经通过包括炎症、增殖和重塑在内的伤口愈合阶段研究了 MC 衍生介质的作用。它们通过释放 TNF-α增强真皮树突细胞中因子 XIIIa 的表达,促进止血和血栓形成,并通过释放炎症介质,包括主要是组胺、VEGF、白细胞介素 (IL)-6 和 IL-8,促进内皮通透性和血管舒张,并促进炎症细胞(主要是单核细胞和中性粒细胞)向损伤部位迁移,有助于血栓稳定。角质形成细胞通过分泌干细胞因子 (SCF) 将 MC 募集到该部位。MC 反过来释放炎症介质,包括主要是组胺、VEGF、白细胞介素 (IL)-6 和 IL-8,有助于增加内皮通透性和血管舒张,并促进炎症细胞(主要是单核细胞和中性粒细胞)迁移到损伤部位。MC 能够激活参与伤口愈合的主要细胞,即成纤维细胞和角质形成细胞。MC 通过 IL-4、血管内皮生长因子 (VEGF) 和碱性成纤维细胞生长因子 (bFGF) 在增殖期刺激成纤维细胞增殖,以产生新的细胞外基质 (ECM)。MC 衍生的介质,包括成纤维细胞生长因子-2、VEGF、血小板衍生生长因子 (PDGF)、TGF-β、神经生长因子 (NGF)、IL-4 和 IL-8,有助于在修复过程中促进新血管生成、纤维蛋白生成或再上皮化。MC 激活抑制和针对 MC 衍生介质的靶向是通过减少炎症反应和瘢痕形成来改善伤口愈合的潜在治疗策略。

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