Platelets can enhance vascular permeability
Platelets can enhance vascular permeability
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DOI：
10.1182/blood-2012-02-413047
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发表时间：
2012-08-09
期刊：
影响因子：
20.3
通讯作者：
Boilard, Eric
中科院分区：
文献类型：
--
作者：
Cloutier, Nathalie;Pare, Alexandre;Boilard, Eric
血小板测量血管，寻找内皮损伤并防止血管完整性的丧失。然而，在某些情况下，血管通透性增加，这表明血小板有时无法实现其预期功能。人类炎症性关节炎与滑膜微血管通透性增强引起的组织水肿有关。鼠类研究表明，这种血管渗漏有助于自身抗体的进入，从而可能促进关节炎症。尽管血小板通常有助于促进微血管的完整性，我们研究了血小板在小鼠实验性关节炎滑膜血管通透性中的作用。使用自身免疫性关节炎的体内模型，我们证实了炎症滑膜中存在内皮间隙。令人惊讶的是，如果没有血小板，发炎关节的通透性就会消失。这种作用是由血小板5-羟色胺通过5-羟色胺转运体积累介导的，并可使用阿托伐他汀特异性再摄取抑制剂抗抑郁药拮抗。与血小板对微血管渗漏的传统作用相反，血小板能够放大和维持渗透性的这一证明增加了血小板的意外功能的快速增长列表。（血。2012;120（6）：1334-1343）
Platelets survey blood vessels, searching for endothelial damage and preventing loss of vascular integrity. However, there are circumstances where vascular permeability increases, suggesting that platelets sometimes fail to fulfill their expected function. Human inflammatory arthritis is associated with tissue edema attributed to enhanced permeability of the synovial microvasculature. Murine studies have suggested that such vascular leak facilitates entry of autoantibodies and may thereby promote joint inflammation. Whereas platelets typically help to promote microvascular integrity, we examined the role of platelets in synovial vascular permeability in murine experimental arthritis. Using an in vivo model of autoimmune arthritis, we confirmed the presence of endothelial gaps in inflamed synovium. Surprisingly, permeability in the inflamed joints was abrogated if the platelets were absent. This effect was mediated by platelet serotonin accumulated via the serotonin transporter and could be antagonized using serotonin-specific reuptake inhibitor antidepressants. As opposed to the conventional role of platelets to microvascular leakage, this demonstration that platelets are capable of amplifying and maintaining permeability adds to the rapidly growing list of unexpected functions for platelets. (Blood. 2012;120(6):1334-1343)