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人牙髓的超微结构和免疫组织化学研究:牙髓内皮细胞中魏尔-帕拉德小体和血管性血友病因子的鉴定

An ultrastructural and immunohistochemical study of human dental pulp: identification of Weibel-Palade bodies and von Willebrand factor in pulp endothelial cells.

作者信息

Jacoby B H, Davis W L, Craig K R, Wagner G, Farmer G R, Harrison J W

机构信息

Department of Periodontics, Baylor College of Dentistry, Dallas, TX.

出版信息

J Endod. 1991 Apr;17(4):150-5. doi: 10.1016/S0099-2399(06)82007-8.

Abstract

Special and specific immunohistochemical techniques as well as routine transmission electron microscopy were used to identify the presence of von Willebrand factor (vWF), a blood clotting factor essential to normal hemostasis, and Weibel-Palade bodies (WPB's), respectively, in the endothelial cells lining the blood vessels from both normal and inflamed human pulpal tissues. In human endothelial cells, WPB's are peculiar and specialized organelles which store vWF. All classes of blood vessels (capillaries, arterioles, arteries, venules, and veins) were vWF positive. The fine structural studies showed similar results with regard to the presence of WPB's. Interestingly, morphometric analyses conducted on the same tissues using either light or transmission electron microscopy showed that significantly more vWF-positive blood vessels were seen in the inflamed tissues. In agreement with the latter observation, transmission electron microscopy showed that more vascular endothelial cells contained WPB's in the inflamed tissues when compared with the normal tissues. From this it appears that during pulpal inflammation, the cascade of events associated with hemostasis may be activated with the increased synthesis and release of vWF by endothelial cells.

摘要

采用特殊且特定的免疫组织化学技术以及常规透射电子显微镜,分别鉴定正常和炎症状态下人类牙髓组织血管内皮细胞中血管性血友病因子(vWF,正常止血所必需的一种凝血因子)和魏尔-帕拉德小体(WPB)的存在情况。在人类内皮细胞中,WPB是储存vWF的特殊细胞器。所有类型的血管(毛细血管、微动脉、动脉、小静脉和静脉)vWF均呈阳性。关于WPB的存在情况,精细结构研究显示了相似的结果。有趣的是,使用光学显微镜或透射电子显微镜对相同组织进行形态计量分析表明,在炎症组织中可见到明显更多的vWF阳性血管。与后一观察结果一致,透射电子显微镜显示,与正常组织相比,炎症组织中有更多的血管内皮细胞含有WPB。由此看来,在牙髓炎症期间,与止血相关的一系列事件可能因内皮细胞合成和释放vWF增加而被激活。

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