...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell cycle >Negative impact of hyperglycaemia on mouse alveolar development
【24h】

Negative impact of hyperglycaemia on mouse alveolar development

机译：高血糖对小鼠肺泡发展的负面影响

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

Diabetes mellitus in pregnancy has been known to affect the embryonic development of various systems, including cardiovascular and nervous systems. However, whether this disease could have a negative impact on embryonic respiratory system remains controversial. In this study, we demonstrated that pregestational diabetes mellitus (PGDM)-induced defects in lung development in mice are mainly characterized by the changes in the morphological structure of the lung. Immunostaining and Western blotting showed that proliferation increased and apoptosis decreased in PGDM. Hyperglycaemia caused pulmonary tissue fibrationas manifested by an increase in Masson staining and decorin expression in PGDM lungs, and the immunofluorescent pro-SPC+ type II pulmonary epithelial cell number was decreased. The alteration of pulmonary epithelial cell differentiation might be due to hyperglycaemia-activated Wnt signalling and suppressed GATA6 expression in PGDM mouse lung tissues and MLE-12 cells. The treatment of MLE-12 cells with high glucose in the presence/absence of XAV939 or su5402 further proved that hyperglycaemia suppressed the expression of GATA6 and pro-SPC by activating Wnt signalling and induced the expression of decorin, -SMA and TGF- by activating Fgf signalling. Therefore, in this study, we revealed that hyperglycemia induced dysfunctional pulmonary cell apoptosis and proliferation, as well as pulmonary myofibroblast hyperplasia, which contributed to the formation of aberrant structure of alveolar walls. Furthermore, the hyperglycaemia also inhibited the differentiation of pulmonary epithelial cells through the canonical Wnt and Fgf signalling, and the alteration of Fgf and Wnt signalling activated TGF-, which would promote the AECII EMT process.
机译：已知糖尿病在妊娠中，已知患有各种系统的胚胎发育，包括心血管和神经系统。然而，这种疾病是否可能对胚胎呼吸系统产生负面影响仍存在争议。在这项研究中，我们证明了小鼠肺部发育中的术糖尿病（PGDM）诱导的缺陷主要是肺形态结构的变化。免疫染色和蛋白质印迹表明，PGDM的增殖增加和细胞凋亡降低。高血糖引起了通过PGDM肺中的Masson染色和装饰蛋白表达的增加表现出的肺组织纤维，并且免疫荧光Pro-SPC + II型肺上皮细胞数减少。肺上皮细胞分化的改变可能是由于高血糖激活的WNT信号传导和PGDM小鼠肺组织和MLE-12细胞中的GATA6表达。在XAV939或SU5402的存在/不存在中处理具有高葡萄糖的MLE-12细胞进一步证明了通过激活WNT信号传导并通过激活诱导菊粉蛋白，-SMA和TGF的表达，抑制高血糖血症和PRO-SPC的表达FGF信号传导。因此，在这项研究中，我们透露，高血糖诱导功能障碍肺细胞凋亡和增殖，以及肺部肌纤维细胞增生，这有助于形成肺泡壁的异常结构。此外，高血糖症还抑制了通过规范WNT和FGF信号传导的肺上皮细胞的分化，以及FGF和WNT信号传导的改变激活TGF-，这将促进AECII EMT过程。

著录项

  • 来源
    《Cell cycle》 |2018年第1期|共12页
  • 作者

    He Mei-yao; Wang Guang; Han Sha-sha; Li Ke; Jin Ya; Liu Meng; Si Zhen-peng; Wang Ju; Liu Guo-sheng; Yang Xuesong;

  • 作者单位

    Jinan Univ Inst Fetal Preterm Labor Med Dept Pediat &

    Neonatol Guangzhou 510630 Guangdong;

    Jinan Univ Coll Med Minist Educ Div Histol &

    Embryol Key Lab Regenerat Med Guangzhou 510632;

    Jinan Univ Inst Fetal Preterm Labor Med Dept Pediat &

    Neonatol Guangzhou 510630 Guangdong;

    Jinan Univ Coll Med Minist Educ Div Histol &

    Embryol Key Lab Regenerat Med Guangzhou 510632;

    Jinan Univ Inst Fetal Preterm Labor Med Dept Pediat &

    Neonatol Guangzhou 510630 Guangdong;

    Jinan Univ Coll Med Minist Educ Div Histol &

    Embryol Key Lab Regenerat Med Guangzhou 510632;

    Jinan Univ Inst Fetal Preterm Labor Med Dept Pediat &

    Neonatol Guangzhou 510630 Guangdong;

    Jinan Univ Inst Biomed Natl Engn Res Ctr Genet Med Guangzhou 510632 Guangdong Peoples R China;

    Jinan Univ Inst Fetal Preterm Labor Med Dept Pediat &

    Neonatol Guangzhou 510630 Guangdong;

    Jinan Univ Coll Med Minist Educ Div Histol &

    Embryol Key Lab Regenerat Med Guangzhou 510632;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    PGDM; Fgf signalling; Wnt signalling; GATA6; EMT;

    机译：PGDM;FGF信号传导;WNT信号;GATA6;EMT;

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