| Literature DB >> 26106824 |
Li-bo Liu1, Xiao-bai Liu2, Jun Ma1, Yun-hui Liu3, Zhi-qing Li1, Teng Ma1, Xi-he Zhao1, Zhuo Xi3, Yi-xue Xue4.
Abstract
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.Entities:
Keywords: Blood-tumor barrier; Bradykinin; Claudin-5; NOS; Occludin; ZONAB
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Year: 2015 PMID： 26106824 DOI： 10.1016/j.bbrc.2015.06.082
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575