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WIF1 causes dysfunction of heart in transgenic mice
Wnt activity is a key regulator of cardiac progenitor cell self-renewal, differentiation and morphogenesis. However, Wnt inhibitory factor 1 (WIF1), a antagonists of Wnt signaling activity, its potential effects on heart development has not yet been approached by either in vivo or in vitro studies....
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835953/ https://www.ncbi.nlm.nih.gov/pubmed/23921644 http://dx.doi.org/10.1007/s11248-013-9738-z |
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author | Lu, Dan Dong, Wei Zhang, Xu Quan, Xiongzhi Bao, Dan Lu, Yingdong Zhang, Lianfeng |
author_facet | Lu, Dan Dong, Wei Zhang, Xu Quan, Xiongzhi Bao, Dan Lu, Yingdong Zhang, Lianfeng |
author_sort | Lu, Dan |
collection | PubMed |
description | Wnt activity is a key regulator of cardiac progenitor cell self-renewal, differentiation and morphogenesis. However, Wnt inhibitory factor 1 (WIF1), a antagonists of Wnt signaling activity, its potential effects on heart development has not yet been approached by either in vivo or in vitro studies. Here, the expression of WIF1 was regulated in a different way in the dilated and hypertrophic cardiomyopathy heart from transgenic mice by mutations in cardiac troponin T, cTnT(R141W) and cTnT(R92Q). The heart tissue specific transgenic mice of WIF1 was studied using M-mode echocardiography and histologic analyses. Production levels of an array of effectors and transcription factors that impact cellular organization and tissue morphology were measured. The effects of WIF1 on β-catenin pathway could be reversed by LiCl regarding signaling pathways and effector and respondent molecules in H9c2 cells, consistent with the expression levels of c-myc, natriuretic peptide precursor type B and skeletal muscle actin α1. Among the most noteworthy findings were that WIF1 impaired the function and structure of heart, and the effects on β-catenin pathway maybe the course of the former. It is anticipated that our findings will contribute to expansion of our understanding of WIF1 biological function on heart development and possible modes of treatment of heart diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11248-013-9738-z) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-3835953 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-38359532013-11-22 WIF1 causes dysfunction of heart in transgenic mice Lu, Dan Dong, Wei Zhang, Xu Quan, Xiongzhi Bao, Dan Lu, Yingdong Zhang, Lianfeng Transgenic Res Original Paper Wnt activity is a key regulator of cardiac progenitor cell self-renewal, differentiation and morphogenesis. However, Wnt inhibitory factor 1 (WIF1), a antagonists of Wnt signaling activity, its potential effects on heart development has not yet been approached by either in vivo or in vitro studies. Here, the expression of WIF1 was regulated in a different way in the dilated and hypertrophic cardiomyopathy heart from transgenic mice by mutations in cardiac troponin T, cTnT(R141W) and cTnT(R92Q). The heart tissue specific transgenic mice of WIF1 was studied using M-mode echocardiography and histologic analyses. Production levels of an array of effectors and transcription factors that impact cellular organization and tissue morphology were measured. The effects of WIF1 on β-catenin pathway could be reversed by LiCl regarding signaling pathways and effector and respondent molecules in H9c2 cells, consistent with the expression levels of c-myc, natriuretic peptide precursor type B and skeletal muscle actin α1. Among the most noteworthy findings were that WIF1 impaired the function and structure of heart, and the effects on β-catenin pathway maybe the course of the former. It is anticipated that our findings will contribute to expansion of our understanding of WIF1 biological function on heart development and possible modes of treatment of heart diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11248-013-9738-z) contains supplementary material, which is available to authorized users. Springer Netherlands 2013-08-07 2013 /pmc/articles/PMC3835953/ /pubmed/23921644 http://dx.doi.org/10.1007/s11248-013-9738-z Text en © The Author(s) 2013 https://creativecommons.org/licenses/by/2.0/ Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. |
spellingShingle | Original Paper Lu, Dan Dong, Wei Zhang, Xu Quan, Xiongzhi Bao, Dan Lu, Yingdong Zhang, Lianfeng WIF1 causes dysfunction of heart in transgenic mice |
title | WIF1 causes dysfunction of heart in transgenic mice |
title_full | WIF1 causes dysfunction of heart in transgenic mice |
title_fullStr | WIF1 causes dysfunction of heart in transgenic mice |
title_full_unstemmed | WIF1 causes dysfunction of heart in transgenic mice |
title_short | WIF1 causes dysfunction of heart in transgenic mice |
title_sort | wif1 causes dysfunction of heart in transgenic mice |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835953/ https://www.ncbi.nlm.nih.gov/pubmed/23921644 http://dx.doi.org/10.1007/s11248-013-9738-z |
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