• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Endothelin-1 expression in vascular adventitial fibroblasts.
【24h】

Endothelin-1 expression in vascular adventitial fibroblasts.

机译：血管外膜成纤维细胞中内皮素-1的表达。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Endothelial cells are a major source of endothelin (ET)-1, but the possibility that vascular adventitial fibroblasts generate ET-1 has not been explored. We hypothesized that aortic adventitial fibroblasts have the ability to produce ET-1, which may contribute to extracellular matrix synthesis. Vascular adventitial fibroblasts were isolated from mouse aorta and incubated with various concentrations of angiotensin II (ANG II). mRNA levels of preproET-1 and type I procollagen were detected with relative RT-PCR. ET-1 levels in culture medium were measured with ELISA. Protein levels of procollagen were detected with Western blotting. ANG II (10 and 100 nM, 1 microM) induced a time- and concentration-dependent increase in preproET-1 mRNA levels (P < 0.05). Induction of preproET-1 mRNA was accompanied by release of immunoreactive peptide ET-1 (P < 0.05). ANG II-evoked increases in preproET-1 mRNA expression and ET-1 release were blocked by losartan (100 microM), an AT1 receptor antagonist, but not PD-123319 (100 microM), an AT2 receptor antagonist. To further confirm our findings, we cloned and then sequenced vascular fibroblast preproET-1 bidirectionally with T7 and M13 reverse sequencing primers. Their nucleotide sequences were identical to preproET-1 cDNA from mouse vascular endothelial cells (accession no. AB081657). Moreover, ANG II-induced type I procollagen mRNA and protein expression were inhibited by BQ-123 (10 microM), an ET(A) receptor inhibitor, but not BQ-788 (10 microM), an ET(B) receptor inhibitor, suggesting a significant role of adventitial ET-1 in regulation of extracellular matrix synthesis. The results demonstrate that vascular adventitial fibroblasts are able to synthesize and release ET-1 in response to ANG II.
机译：内皮细胞是内皮素（ET）-1的主要来源，但尚未探讨血管外膜成纤维细胞产生ET-1的可能性。我们假设主动脉外膜成纤维细胞具有产生ET-1的能力，这可能有助于细胞外基质的合成。从小鼠主动脉中分离出血管外膜成纤维细胞，并与各种浓度的血管紧张素II（ANG II）孵育。用相对RT-PCR检测preproET-1和I型胶原原的mRNA水平。用ELISA测量培养基中的ET-1水平。用蛋白质印迹法检测前胶原蛋白水平。 ANG II（10和100 nM，1 microM）诱导preproET-1 mRNA水平随时间和浓度的增加（P <0.05）。 preproET-1 mRNA的诱导伴随着免疫反应性肽ET-1的释放（P <0.05）。 ANG II引起的preproET-1 mRNA表达和ET-1释放的增加被氯沙坦（100 microM）（一种AT1受体拮抗剂）阻止，但未被PD-123319（100 microM）（一种AT2受体拮抗剂）阻止。为了进一步证实我们的发现，我们克隆了血管成纤维细胞preproET-1，然后用T7和M13反向测序引物双向测序。它们的核苷酸序列与小鼠血管内皮细胞的preproET-1 cDNA相同（登录号AB081657）。此外，ANG II诱导的I型前胶原mRNA和蛋白表达受到ET（A）受体抑制剂BQ-123（10 microM）的抑制，但不受ET（B）受体抑制剂BQ-788（10 microM）的抑制，提示外膜ET-1在调节细胞外基质合成中具有重要作用。结果表明，血管外膜成纤维细胞能够合成和释放对ANG II的ET-1。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号