Bradykinin increased the permeability of BTB via NOS/NO/ZONAB-mediating down-regulation of claudin-5 and occludin

被引：31

作者：

Liu, Li-bo ^{[1
]}

Liu, Xiao-bai ^{[2
]}

Ma, Jun ^{[1
]}

Liu, Yun-hui ^{[3
]}

Li, Zhi-qing ^{[1
]}

Ma, Teng ^{[1
]}

Zhao, Xi-he ^{[1
]}

Xi, Zhuo ^{[3
]}

Xue, Yi-xue ^{[1
]}

机构：

[1] China Med Univ, Coll Basic Med, Dept Neurobiol, Shenyang 110122, Liaoning Provin, Peoples R China

[2] China Med Univ, Year Program 7, Class 96, Shenyang 110122, Peoples R China

[3] China Med Univ, Shengjing Hosp, Dept Neurosurg, Shenyang 110004, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2015年 / 464卷 / 01期

关键词：

Bradykinin; Blood-tumor barrier; NOS; ZONAB; Claudin-5; Occludin; BLOOD-TUMOR BARRIER; NITRIC-OXIDE; FACTOR ZONAB/DBPA; TRANSCRIPTION; BRAIN; ZO-1; EXPRESSION; DELIVERY; CELLS;

D O I：

10.1016/j.bbrc.2015.06.082

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

After demonstrating bradykinin (BK) could increase the permeability of blood-tumor barrier (BTB) via opening the tight junction (TJ), and that the possible mechanism is unclear, we demonstrated that BK could increase the expressions of eNOS and nNOS and promote ZONAB translocation into nucleus. NOS inhibitors L-NAME and 7-NI could effectively block the effect of BK on increasing BTB permeability, decreasing the expressions of claudin-5 and occludin and promoting the translocation of ZONAB. Overexpression of ZONAB could significantly enhance BK-mediating BTB permeability. Meanwhile, chromatin immunoprecipitation verified ZONAB interacted with the promoter of claudin-5 and occludin respectively. This study indicated NOS/NO/ZONAB pathway might be involved in BK's increasing the permeability of BTB. (C) 2015 Elsevier Inc. All rights reserved.

引用

页码：118 / 125

页数：8

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