Plasminogen has been proposed to play an important role in different tissue remodeling processes such as wound healing and tissue regeneration after injuries. The healing of tympanic membrane perforations is a well-organized chain of inflammatory events, with an initial invasion of inflammatory cells followed by reparative and restoration phases. Here we show that the healing of tympanic membrane perforations is completely arrested in plasminogen-deficient mice, with no signs of any healing even 143 days after perforation. Inflammatory cells were recruited to the wounded area, but there were no signs of tissue debridement. In addition, removal of fibrin, keratinocyte migration and in-growth of connective tissue were impaired. This contrasts with skin wound healing, where studies have shown that, although the healing process is delayed, it reaches completion in all plasminogen-deficient mice. Our finding that keratinocyte migration and re-epithelialization were completely arrested in plasminogen-deficient mice indicates that plasminogen/plasmin plays a more profound role in the healing of tympanic membrane perforations than in the healing of other epithelial wounds.

译文

已有建议:纤溶酶原在不同的组织重塑过程中发挥重要作用,例如伤口愈合和受伤后组织再生。鼓膜穿孔的愈合是组织良好的炎症事件链,首先发生炎症细胞入侵,然后进入修复和恢复阶段。在这里,我们显示鼓膜穿孔的愈合在纤溶酶原缺陷型小鼠中完全停止,即使穿孔后143天也没有任何愈合的迹象。炎性细胞被募集到受伤区域,但是没有组织清创的迹象。此外,血纤蛋白的去除,角质形成细胞的迁移和结缔组织的向内生长受到损害。这与皮肤伤口的愈合形成对照,研究表明,尽管愈合过程被延迟,但在所有纤溶酶原缺陷型小鼠中都可以完全愈合。我们的发现,在纤溶酶原缺陷型小鼠中,角质形成细胞的迁移和重新上皮形成被完全阻止,这表明纤溶酶原/纤溶酶在鼓膜穿孔的愈合中比在其他上皮伤口的愈合中起着更重要的作用。

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