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Localization of MMP and TIMP on the chronic skin wounds and possible application of MMP inhibitor

MMP 和 TIMP 在慢性皮肤伤口上的定位以及 MMP 抑制剂的可能应用

基本信息

批准号：
17591871
负责人：
TACHI Masahiro
金额：
$ 2.18万
依托单位：
Tohoku University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17591871/
关键词：
MMP TIMP chronic wound biofilm 褥瘡 MMP阻害薬実験動物虚血皮弁

项目摘要

The functions and regulations of MMPs and MMPs on the wound healing process are not fully understood. The lack of experimental models for chronic wounds is the main problem for the evaluation. We evaluated the functions of MMPs using pressure ulcer tissues. At the edge of epithelization, MMP2 and MMP9 are upregulated in the epithelial cells between basal layer to granular layers. In the middle area of pressure ulcer, MMPs and TIMPs are not found. Along with epithelization, wound fibroblast and wound macrophage expressed MMP2 and MMP9 and TIMP2. For the development of animal model, we evaluated wound healing in the chronic renal failure rat and cinnamon mouse. Delay of wound healing of incisional wound and full thickness wound was not observed in the chronic renal failure rat. Delay in the wound healing was observed in cinnamon mouse. The final study was to observe whether biofilm formation occurs on skin wounds. Full or partial thickness wounds were created on the backs of SD rats. Suspensions of P.aeruginosa (PAO1 carrying the gene encoding the green fluorescent protein) was applied on the wounded area. Wounds were harvested and processed for histology and immunohistochemistry. The presence of biofilm were indicated Rhodamine-conjugated concanavalin A. We confirmed biofilm formation by P.aeruginosa on skin wounds can observe in this experimental model, and partial thickness wounds were proper for to observe biofilm formation. Also, a standardized dorsal ischemic flap was lifted and sutured. Partial thickness wounds were created on the flap. The extent of biofilm formation was significantly diminished on the surface of ischemic wound compared with non-ischemic control. Wound ischemia in the experimental model does not increase the formation of biofilms.

基质金属蛋白酶及其在创伤愈合过程中的作用和调节机制尚不完全清楚。缺乏慢性伤口的实验模型是评估的主要问题。我们使用压疮组织来评估MMPs的功能。在上皮形成的边缘，MMP 2和MMP 9在基底层至颗粒层之间的上皮细胞中上调。随着创面上皮化的进行，沿着创面成纤维细胞和创面巨噬细胞表达MMP 2、MMP 9和TIMP 2。为了建立动物模型，我们在慢性肾功能衰竭大鼠和肉桂小鼠中评价伤口愈合。慢性肾功能衰竭大鼠的切口和全层伤口愈合没有延迟。在肉桂小鼠中观察到伤口愈合延迟。最后一项研究是观察皮肤伤口上是否形成生物膜。在SD大鼠背部造成全层或部分层创伤。将铜绿假单胞菌（携带编码绿色荧光蛋白的基因的PAO 1）的悬浮液施加在创伤区域上。收集伤口并进行组织学和免疫组织化学处理。生物膜的存在表明罗丹明结合刀豆球蛋白A。我们证实在该实验模型中可以观察到铜绿假单胞菌在皮肤伤口上形成生物膜，并且部分厚度伤口适合观察生物膜形成。此外，还提起并缝合了标准化的背侧缺血皮瓣。在皮瓣上形成部分厚度伤口。与非缺血对照相比，缺血伤口表面生物膜形成的程度显著减少。实验模型中的伤口缺血不增加生物膜的形成。