• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Ontogeny of the eotaxins in human lung
【24h】

Ontogeny of the eotaxins in human lung

机译：人类肺中的肠蛋白蛋白的组织发生

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

First published November 30, 2007; doi:10.1152/ajplung.00086.2007.-The ontogeny of the C-C chemo-kines eotaxin~(-1), eotaxm-2, and eotaxin-3 has not been fully elucidated in human lung. We explored a possible role for eotaxin in developing lung by determining the ontogeny of eotaxin~(-1) (CCL11), eotaxin-2 (CCL24), eotaxin-3 (CCL26), and the eotaxin receptor, CCR3. We tested discarded surgical samples of developing human lung tissue using quantitative RT-PCR (QRT-PCR) and immunostaining for expression of CCL11, CCL24, CCL26, and CCR3. We assessed possible functionality of the eotaxin-CCR3 system by treating lung explant cultures with exogenous CCL11 and analyzing the cultures for evidence of changes in proliferation and activation of ERK1/2, a signaling pathway associated with CCR3. QRT-PCR analyses of 22 developing lung tissue samples with gestational ages 10-23 wk demonstrated that eotaxin~(-1) mRNA is most abundant in developing lung, whereas mRNAs for eotaxin-2 and eotaxin-3 are minimally detectable. CCL11 mRNA levels correlated with gestational age (P < 0.05), and immunoreactivity was localized predominantly to airway epithelial cells. QRT-PCR analysis detected CCR3 expression in 16 of 19 developing lung samples. Supporting functional capacity in the immature lung, CCL11 treatment of lung explant cultures resulted in significantly increased (P < 0.05) cell proliferation and activation of the ERK signaling pathway, which is downstream from CCR3, suggesting that proliferation was due to activation of CCR3 receptors by CCL11. We conclude that developing lung expresses the eotaxins and functional CCR3 receptor. CCL11 may promote airway epithelial proliferation in the developing lung.
机译：2007年11月30日第一次出版; DOI：10.1152 / ajplung.00086.2007.- C-C Chemo-kines Eotaxin〜（-1），eotaxm-2和eotaxin-3的Ontogeny尚未在人肺中完全阐明。我们探讨了Eotaxin通过测定Etaxin〜（-1），eotaxin-2（CCl24），eotaxin-3（CCl26）和Eotaxin受体，CCR3的组来产生的肺部开发肺部的作用。我们使用定量RT-PCR（QRT-PCR）和用于表达CCl11，CCL24，CCL26和CCR3的免疫染色来测试丢弃的人肺组织的外科手术样品。我们通过用外源CCl11治疗肺癌蛋白培养物并分析培养物的培养物来评估eTotaxin-CCR3系统的可能功能，以证明ERK1 / 2的增殖和激活的变化，与CCR3相关的信号通路。 QRT-PCR分析22种型肺组织样品具有妊娠期10-23周的牙龈组织样品，表明ETOXIN〜（-1）mRNA在发育肺部最丰富，而ETAXIN-2和ETOTAXIN-3的MRNA是最小的可检测的。 CCL11与妊娠龄（P <0.05）相关的MRNA水平，免疫反应性主要是通气道上皮细胞的定位。 QRT-PCR分析检测到19例肺样品中的16个中的CCR3表达。在不成熟的肺中，CCL11治疗肺癌培养物的CCL11治疗导致了显着增加（P <0.05）细胞增殖和ERK信号通路的激活，其在CCR3下游，表明增殖是由于CCR3受体的激活CCL11。我们得出结论，发展肺表达曙红和功能性CCR3受体。 CCL11可以促进肺炎中的气道上皮增殖。

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