Cannabinoid inhibits HIV-1 Tat-stimulated adhesion of human monocyte-like cells to extracellular matrix proteins.
Cannabinoid inhibits HIV-1 Tat-stimulated adhesion of human monocyte-like cells to extracellular matrix proteins.
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大麻素抑制 HIV-1 Tat 刺激的人类单核细胞样细胞与细胞外基质蛋白的粘附。
DOI：
10.1016/j.lfs.2014.04.008
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发表时间：
2014
期刊：
影响因子：
6.1
通讯作者：
Cabral,GuyA
中科院分区：
文献类型：
--
作者：
Raborn,ErinnS;Jamerson,Melissa;Marciano-Cabral,Francine;Cabral,GuyA
目的本研究旨在评价精选大麻素对人类免疫缺陷病毒1型(HIV-1)反式激活(TAT)蛋白促进单核细胞样细胞与细胞外基质(ECM)蛋白黏附的影响。将人U937单核细胞暴露于含∆9-四氢大麻酚(THc)、CP55,940和其他精选大麻素的TAT中。关键发现THC和CP55,940以与大麻素受体2型(CB2R)连锁的方式抑制TAT增强的U937细胞对ECM蛋白的附着。大麻素对TAT激活的U937细胞的处理与β1整合素表达和聚合肌动蛋白分布的改变有关，提示这些大麻素通过抑制与细胞外基质的黏附而抑制与ECM的黏附。血脑屏障是由细胞元件和细胞外基质组成的复杂结构。HIV-1Tat促进单核细胞跨越这一屏障的迁移，这一过程包括与细胞外基质蛋白的相互作用。结果表明，激活CB2R的大麻素可抑制ECM的黏附过程。因此，这种受体有可能作为一种治疗剂来消融与艾滋病毒引起的单核细胞跨血脑屏障流入相关的神经炎症。
AimsThe aim of this study was to assess the effect of select cannabinoids on human immunodeficiency virus type 1 (HIV-1) transactivating (Tat) protein-enhanced monocyte-like cell adhesion to proteins of the extracellular matrix (ECM).Main methodsCollagen IV, laminin, or an ECM gel was used to construct extracellular matrix layers. Human U937 monocyte-like cells were exposed to Tat in the presence of ∆9-tetrahydrocannabinol (THC), CP55,940, and other select cannabinoids. Cell attachment to ECM proteins was assessed using an adhesion assay.Key findingsTHC and CP55,940 inhibited Tat-enhanced attachment of U937 cells to ECM proteins in a mode that was linked to the cannabinoid receptor type 2 (CB2R). The cannabinoid treatment of Tat-activated U937 cells was associated with altered β1-integrin expression and distribution of polymerized actin, suggesting a modality by which these cannabinoids inhibited adhesion to the ECM.SignificanceThe blood–brain barrier (BBB) is a complex structure that is composed of cellular elements and an extracellular matrix (ECM). HIV-1 Tat promotes transmigration of monocytes across this barrier, a process that includes interaction with ECM proteins. The results indicate that cannabinoids that activate the CB2R inhibit the ECM adhesion process. Thus, this receptor has potential to serve as a therapeutic agent for ablating neuroinflammation associated with HIV-elicited influx of monocytes across the BBB.
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