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缺乏凝血酶受体PAR1的小鼠皮肤伤口愈合正常。

Mice lacking the thrombin receptor, PAR1, have normal skin wound healing.

作者信息

Connolly A J, Suh D Y, Hunt T K, Coughlin S R

机构信息

Department of Pathology, University of California, San Francisco 94143-0130, USA.

出版信息

Am J Pathol. 1997 Nov;151(5):1199-204.

PMID:9358744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1858088/
Abstract

Thrombin's actions on platelets, macrophages, fibroblasts, and endothelial cells have prompted the hypothesis that thrombin may be important for inflammatory and fibroproliferative processes in wound healing. Protease-activated receptor 1 (PAR1) is a G-protein-coupled receptor that mediates many of the cellular activities of thrombin. To test the role of this receptor in vivo, we generated PAR1-deficient mice. Despite the observation that fibroblasts cultured from these mice lacked responsiveness to thrombin in vitro, we now report that there was no difference detected between wild-type and PAR1-deficient mice in skin wound healing assays including time to closure of open wounds, tensile strength of healed incisional wounds, wound histology, and hydroxyproline/DNA content of wound implants. We conclude that PAR1 is not necessary for normal skin wound healing in mice.

摘要

凝血酶对血小板、巨噬细胞、成纤维细胞和内皮细胞的作用引发了一种假说,即凝血酶可能在伤口愈合的炎症和纤维增生过程中起重要作用。蛋白酶激活受体1(PAR1)是一种G蛋白偶联受体,介导凝血酶的许多细胞活性。为了在体内测试该受体的作用,我们培育出了PAR1基因缺陷小鼠。尽管观察到从这些小鼠分离培养的成纤维细胞在体外对凝血酶缺乏反应性,但我们现在报告,在包括开放性伤口闭合时间、愈合切口伤口的抗张强度、伤口组织学以及伤口植入物的羟脯氨酸/DNA含量等皮肤伤口愈合试验中,野生型小鼠和PAR1基因缺陷小鼠之间未检测到差异。我们得出结论,PAR1对小鼠正常皮肤伤口愈合并非必需。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e2/1858088/13bf9cb96b73/amjpathol00023-0031-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e2/1858088/13bf9cb96b73/amjpathol00023-0031-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e2/1858088/13bf9cb96b73/amjpathol00023-0031-a.jpg

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