PDF(Pubmed)
Abstract：
The skin wound healing process consists of hemostatic, inflammatory, proliferative, and maturation phases, with a complex cellular response by multiple cell types in the epidermis, dermis, and immune system. Magnesium is a mineral essential for life, and although magnesium treatment promotes cutaneous wound healing, the molecular mechanism and timing of action of the healing process are unknown. This study, using human epidermal-derived HaCaT cells and human normal epidermal keratinocyte cells, was performed to investigate the mechanism involved in the effect of magnesium on wound healing. The expression levels of epidermal differentiation-promoting factors were reduced by MgCl2, suggesting an inhibitory effect on epidermal differentiation in the remodeling stage of the late wound healing process. On the other hand, MgCl2 treatment increased the expression of matrix metalloproteinase-7 (MMP7), a cell migration-promoting factor, and enhanced cell migration via the MEK/ERK pathway activation. The enhancement of cell migration by MgCl2 was inhibited by MMP7 knockdown, suggesting that MgCl2 enhances cell migration which is mediated by increased MMP7 expression. Our results revealed that MgCl2 inhibits epidermal differentiation but promotes cell migration, suggesting that applying magnesium to the early wound healing process could be beneficial.
摘要：
皮肤伤口愈合过程包括止血，炎症，增殖性,和成熟阶段，表皮中多种细胞类型的复杂细胞反应，真皮,和免疫系统。镁是生命必需的矿物质,虽然镁治疗促进皮肤伤口愈合，愈合过程的分子机制和作用时间尚不清楚。这项研究,使用人表皮来源的HaCaT细胞和人正常表皮角质形成细胞，进行研究以研究镁对伤口愈合的影响所涉及的机制。MgCl2降低了表皮分化促进因子的表达水平，表明在晚期伤口愈合过程的重塑阶段对表皮分化有抑制作用。另一方面,MgCl2处理增加基质金属蛋白酶-7(MMP7)的表达,细胞迁移促进因子,并通过MEK/ERK途径激活增强细胞迁移。MMP7敲低抑制MgCl2对细胞迁移的增强，表明MgCl2增强由MMP7表达增加介导的细胞迁移。我们的结果表明，MgCl2抑制表皮分化，但促进细胞迁移，这表明将镁应用于早期伤口愈合过程可能是有益的。
