Inhibition of proteoglycan synthesis in human endothelial cells after infection with herpes simplex virus type 1 in vitro.
Inhibition of proteoglycan synthesis in human endothelial cells after infection with herpes simplex virus type 1 in vitro.
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DOI：
10.1165/ajrcmb/2.5.423
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发表时间：
1990-05
影响因子：
6.4
通讯作者：
R. Kaner;R. Iozzo;Z. Ziaie;N. A. Kefalides
中科院分区：
文献类型：
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作者：
R. Kaner;R. Iozzo;Z. Ziaie;N. A. Kefalides
以单纯疱疹病毒1型（HSV-1）感染人内皮细胞作为内皮细胞损伤模型，研究HSV-1感染对人内皮细胞蛋白多糖合成的影响。用HSV-1以0.001至1.0的感染复数感染来自人脐静脉的早期传代内皮细胞的汇合培养物。HSV-1感染产生了高达85%的总蛋白多糖合成的剂量依赖性抑制。尽管与软骨素/硫酸皮肤素蛋白聚糖相比，引起硫酸乙酰肝素50%抑制所需的病毒量增加了2- 3倍，但即使在高病毒剂量下，抑制作用也相对平行。未抑制硫酸化硫酸乙酰肝素蛋白聚糖，其含有比主要种属短的糖胺聚糖链。结果表明，HSV-1感染人内皮细胞对宿主细胞代谢产生复杂的影响。病毒诱导的蛋白多糖代谢变化可能影响细胞-基质相互作用，并导致血管壁功能改变。
The effects of herpes simplex virus type 1 (HSV-1) infection on proteoglycan synthesis by human endothelial cells were studied as a model of endothelial cell injury. Confluent cultures of early passage endothelial cells from human umbilical vein were infected with HSV-1 at multiplicities of infection from 0.001 to 1.0. HSV-1 infection produced a dose-dependent inhibition of total proteoglycan synthesis of up to 85%. Although there was a 2- to 3-fold increase in the quantity of virus necessary to cause 50% inhibition of heparan sulfate compared to chondroitin/dermatan sulfate proteoglycan, the inhibition was relatively parallel, even up to high virus doses. There was no inhibition of an undersulfated heparan sulfate proteoglycan that contained glycosaminoglycan chains shorter than the predominant species. The results indicate that HSV-1 infection of human endothelial cells produces complex effects on host-cell metabolism. The viral-induced changes in proteoglycan metabolism may influence cell-matrix interactions and lead to altered vessel wall function.