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2
Protease-activated receptor-1 antagonist F 16618 reduces arterial restenosis by down-regulation of tumor necrosis factor α and matrix metalloproteinase 7 expression, migration, and proliferation of vascular smooth muscle cells.蛋白酶激活受体-1 拮抗剂 F 16618 通过下调肿瘤坏死因子 α 和基质金属蛋白酶 7 的表达，抑制血管平滑肌细胞的迁移、增殖，从而减少动脉再狭窄。
J Pharmacol Exp Ther. 2011 Mar;336(3):643-51. doi: 10.1124/jpet.110.175182. Epub 2010 Dec 7.
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Protease-activated receptors mediate crosstalk between coagulation and fibrinolysis.蛋白酶激活受体介导凝血和纤溶之间的串扰。
Blood. 2010 Dec 2;116(23):5037-44. doi: 10.1182/blood-2010-06-293126. Epub 2010 Aug 24.
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Protease-activated receptor 2 deficiency reduces cardiac ischemia/reperfusion injury.蛋白酶激活受体 2 缺乏可减少心脏缺血/再灌注损伤。
Arterioscler Thromb Vasc Biol. 2010 Nov;30(11):2136-42. doi: 10.1161/ATVBAHA.110.213280. Epub 2010 Aug 19.
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PAR1 and PAR2 couple to overlapping and distinct sets of G proteins and linked signaling pathways to differentially regulate cell physiology.PAR1 和 PAR2 与重叠且不同的 G 蛋白和相关信号通路偶联，以差异调节细胞生理。
Mol Pharmacol. 2010 Jun;77(6):1005-15. doi: 10.1124/mol.109.062018. Epub 2010 Mar 9.
6
Platelet matrix metalloprotease-1 mediates thrombogenesis by activating PAR1 at a cryptic ligand site.血小板基质金属蛋白酶-1通过在隐蔽配体位点激活PAR1来介导血栓形成。
Cell. 2009 Apr 17;137(2):332-43. doi: 10.1016/j.cell.2009.02.018.
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PAR-2 mediates increased inflammatory cell adhesion and neointima formation following vascular injury in the mouse.蛋白酶激活受体-2介导小鼠血管损伤后炎症细胞黏附增加及新生内膜形成。
Atherosclerosis. 2008 May;198(1):57-64. doi: 10.1016/j.atherosclerosis.2007.09.043. Epub 2007 Nov 9.
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Protease-activated receptor-1 contributes to cardiac remodeling and hypertrophy.蛋白酶激活受体-1促进心脏重塑和肥大。
Circulation. 2007 Nov 13;116(20):2298-306. doi: 10.1161/CIRCULATIONAHA.107.692764. Epub 2007 Oct 29.
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'Role reversal' for the receptor PAR1 in sepsis-induced vascular damage.脓毒症诱导的血管损伤中受体PAR1的“角色反转”
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蛋白酶激活受体 2 调节蛋白酶激活受体 1 驱动的新生内膜增生。

Protease-activated receptor-2 modulates protease-activated receptor-1-driven neointimal hyperplasia.

机构信息

Hemostasis and Thrombosis Laboratory, Molecular Oncology Research Institute, Tufts Medical Center, 75 Kneeland St, Boston, MA 02111, USA.

出版信息

Arterioscler Thromb Vasc Biol. 2011 Dec;31(12):e100-6. doi: 10.1161/ATVBAHA.111.238261. Epub 2011 Sep 22.

DOI:10.1161/ATVBAHA.111.238261
PMID:21940952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3241440/
Abstract

OBJECTIVE

Emerging evidence suggests that protease-activated receptors-1 and -2 (PAR1 and PAR2) can signal together in response to proteases found in the rapidly changing microenvironment of damaged blood vessels. However, it is unknown whether PAR1 and PAR2 promote or mitigate the hyperplastic response to arterial injury. Using cell-penetrating PAR1 pepducins and mice deficient in PAR1 or PAR2, we set out to determine the respective contributions of the receptors to hyperplasia and phenotypic modulation of smooth muscle cells (SMCs) in response to arterial injury.

METHODS AND RESULTS

SMCs were strongly activated by PAR1 stimulation, as evidenced by increased mitogenesis, mitochondrial activity, and calcium mobilization. The effects of chronic PAR1 stimulation following vascular injury were studied by performing carotid artery ligations in mice treated with the PAR1 agonist pepducin, P1pal-13. Histological analysis revealed that PAR1 stimulation caused striking hyperplasia, which was ablated in PAR1(-/-) and, surprisingly, PAR2(-/-) mice. P1pal-13 treatment yielded an expression pattern consistent with a dedifferentiated phenotype in carotid artery SMCs. Detection of PAR1-PAR2 complexes provided an explanation for the hyperplastic effects of the PAR1 agonist requiring the presence of both receptors.

CONCLUSIONS

We conclude that PAR2 regulates the PAR1 hyperplastic response to arterial injury leading to stenosis.

摘要

目的

新出现的证据表明，蛋白酶激活受体-1 和 -2（PAR1 和 PAR2）可以在响应损伤血管中快速变化的微环境中的蛋白酶时协同发出信号。然而，尚不清楚 PAR1 和 PAR2 是否促进或减轻动脉损伤后的过度增生反应。使用穿透细胞的 PAR1 pepducin 和 PAR1 或 PAR2 缺失的小鼠，我们着手确定受体各自对平滑肌细胞（SMC）对动脉损伤的过度增生和表型调节的贡献。

方法和结果

PAR1 刺激强烈激活 SMC，表现为有丝分裂增加、线粒体活性和钙动员增加。通过用 PAR1 激动剂 pepducin，P1pal-13 处理的小鼠进行颈动脉结扎来研究血管损伤后 PAR1 的慢性刺激的影响。组织学分析显示 PAR1 刺激引起明显的过度增生，在 PAR1（-/-）和令人惊讶的 PAR2（-/-）小鼠中被消除。P1pal-13 处理产生了与颈动脉 SMC 去分化表型一致的表达模式。PAR1-PAR2 复合物的检测为需要两种受体存在的 PAR1 激动剂的过度增生效应提供了一种解释。

结论

我们得出结论，PAR2 调节 PAR1 对动脉损伤的过度增生反应，导致狭窄。