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缓激肽通过黑素瘤细胞中的激肽 B2 受体增加内皮素-1 的分泌和表达。

Bradykinin increases the secretion and expression of endothelin-1 through kinin B2 receptors in melanoma cells.

机构信息

Department of Applied Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.

出版信息

Peptides. 2010 Feb;31(2):238-41. doi: 10.1016/j.peptides.2009.12.003. Epub 2009 Dec 5.

DOI:10.1016/j.peptides.2009.12.003
PMID:19969036
Abstract

The present study was conducted to determine whether bradykinin would affect the secretion and expression of endothelin-1 (ET-1) in B16-BL6 melanoma cells. Bradykinin administered to cultured melanoma cells increased preproET-1 mRNA level and the secretion of ET-1. Although kinin B(1) and B(2) receptor mRNAs are expressed in the melanoma cells, the increase of preproET-1 mRNA expression and the secretion of ET-1 were inhibited by kinin B(2), but not by B(1), receptor antagonist. These results suggest that bradykinin regulates the secretion and biosynthesis of ET-1 through kinin B(2) receptor in tumor cells, especially melanoma cells.

摘要

本研究旨在探讨缓激肽是否会影响 B16-BL6 黑色素瘤细胞内皮素-1(ET-1)的分泌和表达。给予培养的黑色素瘤细胞缓激肽可增加前 ET-1mRNA 水平和 ET-1 的分泌。虽然黑色素瘤细胞中表达激肽 B(1)和 B(2)受体 mRNA,但 ET-1 的前体 mRNA 表达增加和分泌被激肽 B(2)受体拮抗剂而非 B(1)受体拮抗剂抑制。这些结果表明,缓激肽通过肿瘤细胞,特别是黑色素瘤细胞中的激肽 B(2)受体调节 ET-1 的分泌和生物合成。

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