Cardiac ion channels associated with unexplained stillbirth - an immunohistochemical study

与不明原因死产相关的心脏离子通道——免疫组织化学研究

阅读:11
作者:Susana Quesado Branco, Gauri Batra, Gemma Petts, Ainslie Hancock, Alan Kerby, Chloe Anne Brady, Alexander E P Heazell

Conclusions

Two ion channels associated with channelopathies demonstrated lower levels of expression in cases of unexplained stillbirth. Further genetic studies using human tissue should be performed to understand the association between channelopathies and otherwise unexplained stillbirths.

Methods

A case control study was conducted using formalin-fixed cardiac tissue from 20 cases of unexplained stillbirth and a control group of 20 cases of stillbirths from intrapartum hypoxia. 4 µm tissue sections were stained using haematoxylin and eosin, Masson's trichrome (MT) and Elastic van Gieson (EVG). Immunohistochemistry (IHC) was performed using antibodies against CACNA1G, KCNJ2, KCNQ1, KCNH2 and KCNE1. The cardiac conduction system in samples stained with MT and EVG could not be identified. Therefore, the levels of immunoperoxidase staining were quantified using QuPath software.

Results

The nuclear-cytoplasmic ratio of sections stained with haematoxylin and eosin was higher for the hypoxia group (hypoxia median 0.13 vs. 0.04 unexplained, p < 0.001). CACNA1G (unexplained median 0.26 vs. hypoxia 0.30, p=0.009) and KCNJ2 (unexplained median 0.35 vs. hypoxia 0.41, p=0.001) had lower staining intensity in the unexplained stillbirth group. There were no statistically significant differences in the staining intensity of KCNQ1, KCNH2 and KCNE1. Conclusions: Two ion channels associated with channelopathies demonstrated lower levels of expression in cases of unexplained stillbirth. Further genetic studies using human tissue should be performed to understand the association between channelopathies and otherwise unexplained stillbirths.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。