欢迎您！东篱公司
退出
-
申报数据库
-
立项数据库
-
成果数据库
-
项目获奖数据库
中文摘要：
目的探索信号分子蛋白激酶C（protein kinase C，PKC）在内皮一单核细胞激活多肽Ⅱ（endothelial monocyte activating polypeptide—Ⅱ，EMAP—Ⅱ）增强血肿瘤屏障（blood—tumor barrier，BTB）通透性中的作用。方法荷瘤大鼠被随机分成3组C每组8只）：对照组、EMAP—Ⅱ组、H7＋EMAP—Ⅱ组。采用伊文思蓝（Evans blue，EB）渗透性实验评估实验各组BTB通透性的变化；Western Blot法、免疫组织化学法及免疫荧光法检测脑微血管内皮细胞上紧密连接相关蛋白occludin表达水平的变化。结果与对照组和H7＋EMAP-Ⅱ组相比较，EMAP—Ⅱ组BTB通透性显著增高，紧密连接相关蛋白occludin的表达水平显著降低，EMAP—Ⅱ的作用受到PKC抑制剂H7预处理的显著抑制。结论信号分子PKC在EMAP—Ⅱ增强BTB通透性中发挥着重要的作用。
英文摘要：
Objective To detect the role and mechanism of protein kinase C（PKC） in the endothelial monocyte-activating polypeptide-Ⅱ（EMAP-Ⅱ） -induced increase in blood-tumorbarrier（BTB） permeability. Methods Tumor-bearing rats were randomly divided into 3 groups（n = 8）： control, EMAP-Ⅱ, and HT＋EMAP-Ⅱ groups. Evans blue（EB） assay was used to evaluate the changes of BTB permeability. The expression of fight junction-related protein occludin in brain microvascular endothelial cells was measured by western blot, immunohistoehemistry and immunofluorescent assays. Results EMAP-Ⅱ significantly increased permeability of the BTB and decreased the expression level of occludin in brain microvascular endothelial cells, pretreatment with H7（the inhibitor of PKC） blocked EMAP-Ⅱ-indueed increase of BTB permeability and inhibited EMAP-Ⅱ-induced downregulation of occludin expression level significantly. Conclusions PKC signaling molecule plays an important role in EMAP-Ⅱ-induced increase in the BTB permeability.
同期刊论文项目
同项目期刊论文
Low-dose Endothelial Monocyte-activating Polypeptide-II Increases Permeability of Blood-tumor Barrie
Overexpression of Roundabout4 predicts poor prognosis of primary glioma patients via correlating wit
MiR-18aincreased the permeability of BTB via RUNX1 mediated down-regulation of ZO-1, occluding and c
C-terminus of Human BKca Channel Alpha Subunit Enhances the Permeability of the Brain Endothelial Ce
MiR-330-Mediated Regulation of SH3GL2 Expression Enhances Malignant Behaviors of Glioblastoma Stem C
Functions for the cAMP/Epac/Rap1 Signaling Pathway in Low-Dose Endothelial Monocyte-Activating Polyp
Signal Mechanisms Underlying Low-Dose Endothelial Monocyte-Activating Polypeptide-II-Induced Opening
Roundabout 4 regulates blood-tumor barrier permeability through the modulation of ZO-1, Occludin, an
Roles of Serine/Threonine Phosphatases in Low-Dose Endothelial Monocyte-Activating Polypeptide-II-In
Low-Dose Endothelial Monocyte-Activating Polypeptide-II Increases Blood-Tumor Barrier Permeability b
Role of cAMP-dependent protein kinase A activity in low-dose endothelial monocyte-activating polypep
MiR-152 functions as a tumor suppressor in glioblastoma stem cellsby targeting Krüppel-like factor 4
miR-34c Regulates the Permeability of Blood-Tumor Barrier via MAZ-Mediated Expression Changes of ZO-
Roundabout4 suppresses glioma-induced endothelial cell proliferation, migration and tube formation i
Endothelial-monocyte-activating polypeptide II induces rat C6 glioma cell apoptosis via the mitochon
Low-dose endothelial monocyte-activating polypeptide-II increases permeability of blood–tumor barrie
Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cell
CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regu
Prognostic significance of osteopontin and carbonic anhydrase 9 in human brain tumors: A Meta-Analys
MiR-449a exerts tumor-suppressive functions in human glioblastoma by targeting Myc-associated zinc-f
CRM197 in combination with shRNA interference of VCAM-1 displays enhanced inhibitory effects on huma
MiR-18a increased the permeability of BTB via RUNX1 mediated down-regulation of ZO-1, occludin and c
Low-Frequency Ultrasound Irradiation Increases Blood-Tumor Barrier Permeability by Transcellular Pat
期刊信息
位置：