PDF(Pubmed)
Abstract：
UNASSIGNED: The primary goals of this study were to investigate the potential roles of ZNF22 and HDAC3 as a histone deacetylase in regulating an increases in blood-tumor barrier (BTB) permeability and some of the possible molecular mechanisms associated with this effect.
UNASSIGNED: The expression of ZNF22 and HDAC3 in glioma-exposed endothelial cells (GECs) of BTB were detected transcription real-time PCR or western blot. The interaction of ZNF22 and HDAC3 in GECs associated with transcript effect was analyzed by means of Co-Immunoprecipitation and luciferase reporter assay.
UNASSIGNED: In the present investigation, GECs expressed higher levels of ZNF22 as a zinc finger transcription factor and HDAC3 than endothelial cells. We then affirmed that silencing HDAC3 or ZNF22 led to a reduction in BTB permeability. By bioinformatics analysis, chromatin immunoprecipitation (ChIP) assays and luciferase assay, we found that ZNF22 had a target binding relationship with the promoter regions of ZO-1, Occludin, and Claudin-5 and negatively regulated the expression of ZO-1, Occludin, and Claudin-5. Furthermore, we revealed that HDAC3, as a co-transcript repressor with histone deacetylase activity, could interact with ZNF22 to hinder the expression of TJ-associated proteins, thereby further facilitating the permeability of BTB.
UNASSIGNED: ZNF22 acted as a transcription factor in conjunction with HDAC3 to modulate the expression of TJ-associated proteins, which was correlated with an increase in BTB permeability. These results may provide new strategies and targets for the chemotherapy of gliomas as well as intracranial infections.
UNASSIGNED: The expression of ZNF22 and HDAC3 in glioma-exposed endothelial cells (GECs) of BTB were detected transcription real-time PCR or western blot. The interaction of ZNF22 and HDAC3 in GECs associated with transcript effect was analyzed by means of Co-Immunoprecipitation and luciferase reporter assay.
UNASSIGNED: In the present investigation, GECs expressed higher levels of ZNF22 as a zinc finger transcription factor and HDAC3 than endothelial cells. We then affirmed that silencing HDAC3 or ZNF22 led to a reduction in BTB permeability. By bioinformatics analysis, chromatin immunoprecipitation (ChIP) assays and luciferase assay, we found that ZNF22 had a target binding relationship with the promoter regions of ZO-1, Occludin, and Claudin-5 and negatively regulated the expression of ZO-1, Occludin, and Claudin-5. Furthermore, we revealed that HDAC3, as a co-transcript repressor with histone deacetylase activity, could interact with ZNF22 to hinder the expression of TJ-associated proteins, thereby further facilitating the permeability of BTB.
UNASSIGNED: ZNF22 acted as a transcription factor in conjunction with HDAC3 to modulate the expression of TJ-associated proteins, which was correlated with an increase in BTB permeability. These results may provide new strategies and targets for the chemotherapy of gliomas as well as intracranial infections.
摘要：
UNASSIGNED：本研究的主要目标是研究ZNF22和HDAC3作为组蛋白脱乙酰酶在调节血肿瘤屏障（BTB）通透性增加中的潜在作用，以及与这种作用相关的一些可能的分子机制。
UNASSIGNED：用转录实时PCR或westernblot检测BTB胶质瘤暴露内皮细胞（GECs）中ZNF22和HDAC3的表达。通过免疫共沉淀和荧光素酶报告基因测定分析了ZNF22和HDAC3在GECs中与转录效应相关的相互作用。
未经批准：在本次调查中，GECs比内皮细胞表达更高水平的ZNF22作为锌指转录因子和HDAC3。然后我们确认沉默HDAC3或ZNF22导致BTB渗透性降低。通过生物信息学分析,染色质免疫沉淀（ChIP）测定和荧光素酶测定，我们发现ZNF22与ZO-1、Occludin、和Claudin-5负调控ZO-1，Occludin，还有Claudin-5.此外，我们揭示了HDAC3作为具有组蛋白去乙酰化酶活性的共转录阻遏物，可以与ZNF22相互作用，阻碍TJ相关蛋白的表达，从而进一步促进BTB的渗透性。
UNASSIGNED：ZNF22与HDAC3一起作为转录因子调节TJ相关蛋白的表达，这与BTB通透性的增加有关。这些结果可能为胶质瘤和颅内感染的化疗提供新的策略和目标。
UNASSIGNED：用转录实时PCR或westernblot检测BTB胶质瘤暴露内皮细胞（GECs）中ZNF22和HDAC3的表达。通过免疫共沉淀和荧光素酶报告基因测定分析了ZNF22和HDAC3在GECs中与转录效应相关的相互作用。
未经批准：在本次调查中，GECs比内皮细胞表达更高水平的ZNF22作为锌指转录因子和HDAC3。然后我们确认沉默HDAC3或ZNF22导致BTB渗透性降低。通过生物信息学分析,染色质免疫沉淀（ChIP）测定和荧光素酶测定，我们发现ZNF22与ZO-1、Occludin、和Claudin-5负调控ZO-1，Occludin，还有Claudin-5.此外，我们揭示了HDAC3作为具有组蛋白去乙酰化酶活性的共转录阻遏物，可以与ZNF22相互作用，阻碍TJ相关蛋白的表达，从而进一步促进BTB的渗透性。
UNASSIGNED：ZNF22与HDAC3一起作为转录因子调节TJ相关蛋白的表达，这与BTB通透性的增加有关。这些结果可能为胶质瘤和颅内感染的化疗提供新的策略和目标。
