Adenoviral gene transfer of viral interleukin-10 protects cerebrovascular impairment induced by lysophosphatidylcholine.
Adenoviral gene transfer of viral interleukin-10 protects cerebrovascular impairment induced by lysophosphatidylcholine.
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病毒白细胞介素 10 的腺病毒基因转移可保护溶血磷脂酰胆碱引起的脑血管损伤。
DOI：
10.1016/j.ejphar.2007.10.047
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发表时间：
2008-02
影响因子：
5
通讯作者：
中科院分区：
文献类型：
--
作者：
脑血管疾病是世界范围内发病率和死亡率的重要原因。炎症过程诱导多种病理反应，例如动脉粥样硬化，其在缺血性脑血管病的病因学和脑缺血的病理生理学中在中风中具有基本作用。病毒性白细胞介素-10（viral interleukin-10，vIL-10）是一种潜在的抗炎细胞因子，已被广泛研究。然而，vIL-10对脑血管功能障碍的疗效尚不清楚。本研究旨在探讨腺病毒介导的vIL-10基因转移（Ad/vIL-10）对脑血管功能的影响。为进一步阐明基底动脉收缩与细胞粘附及粘附分子的关系，本实验采用lysoPC孵育培养的微血管内皮细胞bEnd.3，观察Ad/vIL-10对单核细胞-脑血管内皮细胞粘附及细胞粘附分子表达的影响。我们的结果表明，Ad/vIL-10显着降低由lysoPC引起的基底主动脉收缩反应，并增强血管对乙酰胆碱的舒张作用。进一步的研究表明Ad/vIL-10可显著抑制单核细胞与脑血管内皮细胞的粘附，并抑制炎症过程中的生物标志物细胞间粘附分子-1（ICAM-1）和血管细胞粘附分子-1（VCAM-1）的上调。这些结果表明Ad/vIL-10对炎症诱导的脑血管功能障碍具有保护作用，并证明抑制细胞粘附分子的表达可能是vIL-10在炎症过程中保护血管功能的途径之一。
Cerebrovascular disease is a significant cause of morbidity and mortality in the world. Inflammatory processes induce several pathological responses such as atherosclerosis, which have fundamental roles in stroke in the etiology of ischemic cerebrovascular disease and the pathophysiology of cerebral ischemia. Viral interleukin-10 (vIL-10), a potential anti-inflammatory cytokine, has been studied extensively. However, the efficacy of vIL-10 on cerebrovascular dysfunction is not well known. Our goal in this study was to explore the effect of gene transfer of vIL-10 mediated by adenovirus (Ad/vIL-10) on cerebrovascular function using a model of vasocontraction of isolated basilar artery from mongrel dogs induced by lysophosphatidylcholine (lysoPC), a proinflammatory and atherogenic serum lysophospholipid. To clarify the relation between contraction of basilar aorta and cell adhesion and adhesion molecules, our further study explored effects of Ad/vIL-10 on monocyte-cerebrovascular endothelial cells adhesion and expression of cell adhesion molecule by cultured cerebromicrovascular endothelial cells, bEnd.3, after incubation by lysoPC. Our results showed that Ad/vIL-10 significantly decreased contractive response of basilar aorta produced by lysoPC and augmented vasorelaxation to acetylcholine. Further studies showed the Ad/vIL-10 significantly depressed adherence of monocytes to cerebrovascular endothelial cells and inhibited up-regulation of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) which are bio-markers in inflammatory progress. These data demonstrated the protective effects of Ad/vIL-10 on cerebrovascular dysfunction induced by inflammation, and proved that inhibition of expression of cell adhesion molecules should be one of ways of vIL-10 to protect vascular function during inflammation.
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影响因子：
2.9
作者：
Rothoerl, Ralf Dirk;Schebesch, Karl-Michael;Pina, Ana-Luisa
通讯作者：
Pina, Ana-Luisa
DOI：
10.1161/01.atv.0000015903.02749.71
发表时间：
2002-05-01
影响因子：
8.7
作者：
Yamakawa, T;Tanaka, S;Eguchi, S
通讯作者：
Eguchi, S
影响因子：
2.6
作者：
T. Verbeuren
通讯作者：
T. Verbeuren
影响因子：
3
作者：
Chan, H;Lougheed, F;Steinbrecher, UP
通讯作者：
Steinbrecher, UP
DOI：
10.1002/9783527692156.ch49
发表时间：
2017-10
期刊：
--
影响因子：
--
作者：
M. Lauterbach;L. Labzin;E. Latz
通讯作者：
M. Lauterbach;L. Labzin;E. Latz