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首页> 外文期刊>Journal of Pathology: Journal of the Pathological Society of Great Britain and Ireland >Human ageing impairs injury-induced in vivo expression of tissue inhibitor of matrix metalloproteinases (TIMP)-1 and -2 proteins and mRNA.
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Human ageing impairs injury-induced in vivo expression of tissue inhibitor of matrix metalloproteinases (TIMP)-1 and -2 proteins and mRNA.

机译：人的衰老损害了损伤诱导的基质金属蛋白酶（TIMP）-1和-2蛋白和mRNA组织抑制剂的体内表达。

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摘要

Proteolysis is an essential component of wound healing but, if uncontrolled, it may lead to degradation of the neo-matrix and a delay in wound repair. Despite numerous reports of impaired wound healing associated with increasing age, the control of proteolysis is completely unknown. Tissue inhibitor of matrix metalloproteinases (TIMP)-1 and -2 inhibit the activity of matrix metalloproteinases and the pattern of regulation of these molecules determines in part the spatial and temporal regulation of proteolytic activity. This study reports on TIMP-1 and -2 protein localization using immunocytochemistry in healing wounds of healthy subjects of different ages from day 1 to 6 months post-wounding, and has quantified the mRNA levels for both inhibitors using reverse transcriptase-polymerase chain reaction (RT-PCR). TIMP-1 and TIMP-2 proteins are up-regulated from 24 h post-wounding, with a decrease in staining intensity by day 7 for TIMP-2 and by day 14 for TIMP-1. Steady-state mRNA levels for both TIMPs were significantly greater in normal young skin than in aged skin. In the young, there was a significant increase in mRNA expression for TIMP-1 and -2 by day 3 post-wounding, which decreased by day 14 and had returned to basal levels at day 21. In the wounds of the aged subjects, basal levels were observed for TIMP-1 and -2 at all time-points. These results suggest that intrinsic cutaneous ageing is associated with reduced levels of TIMP mRNA both in normal skin and during acute wound repair. These levels may be instrumental in dermal tissue breakdown in normal skin, retarded wound healing, and the predisposition of the elderly to chronic wound healing states.
机译：蛋白水解是伤口愈合的重要组成部分，但如果不受控制，则可能导致新基质降解并延缓伤口修复。尽管有许多报道说随着年龄的增长伤口愈合不良，但是蛋白水解的控制还是完全未知的。基质金属蛋白酶的组织抑制剂（TIMP）-1和-2抑制基质金属蛋白酶的活性，这些分子的调节方式在一定程度上决定了蛋白水解活性的时空调节。这项研究报告了在免疫后1到6个月内不同年龄健康受试者的伤口中使用免疫细胞化学对TIMP-1和-2蛋白进行定位的情况，并使用逆转录酶-聚合酶链反应对两种抑制剂的mRNA水平进行了定量分析（ RT-PCR）。从受伤后24小时开始，TIMP-1和TIMP-2蛋白被上调，TIMP-2的染色强度在第7天下降，TIMP-1的染色强度在第14天下降。在正常的年轻皮肤中，两种TIMP的稳态mRNA水平均显着高于老年皮肤。在年轻人中，受伤后第3天TIMP-1和-2的mRNA表达显着增加，到第14天下降，并在第21天恢复到基础水平。在老年受试者的伤口中，基础在所有时间点均观察到TIMP-1和-2的水平。这些结果表明，固有的皮肤衰老与正常皮肤和急性伤口修复过程中TIMP mRNA水平降低有关。这些水平可能有助于正常皮肤的真皮组织破裂，伤口愈合迟缓以及老年人易患慢性伤口愈合状态。

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