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The defects in development and apoptosis of cardiomyocytes in mice lacking the transcriptional factor Pax-8

Cardiac-specific deletion of ALK3 is lethal in mid-gestation with ventricular septum malformations (VSM). This study was designed to define the Pax-8's role in heart development and cardiomyocyte apoptosis. Pathologic changes in the hearts of Pax-8 or ALK3 knockout and wild type control mice were de... Full description

Journal Title: International Journal of Cardiology 12 January 2012, Vol.154(1), pp.43-51
Main Author: Yang, Deye
Other Authors: Lai, Dandan , Huang, Xiaoyan , Shi, Xiangxiang , Gao, Zhan , Huang, Fang , Zhou, Xi , Geng, Yong-Jian
Format: Electronic Article Electronic Article
Language: English
Subjects:
Vsm
Bmp
Dab
Pfa
Hrp
Ubm
ID: ISSN: 0167-5273 ; E-ISSN: 1874-1754 ; DOI: 10.1016/j.ijcard.2010.08.057
Link: http://dx.doi.org/10.1016/j.ijcard.2010.08.057
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recordid: elsevier_sdoi_10_1016_j_ijcard_2010_08_057
title: The defects in development and apoptosis of cardiomyocytes in mice lacking the transcriptional factor Pax-8
format: Article
creator:
  • Yang, Deye
  • Lai, Dandan
  • Huang, Xiaoyan
  • Shi, Xiangxiang
  • Gao, Zhan
  • Huang, Fang
  • Zhou, Xi
  • Geng, Yong-Jian
subjects:
  • Ventricular Septum Malformations
  • Pax-8
  • Gene
  • Bone Morphogenetic Protein Receptor
  • Vsm
  • Bmp
  • Bmpr
  • Alk3
  • Pax-8
  • Tunel
  • Tgfβ
  • Dab
  • Pfa
  • Hrp
  • Ubm
  • Pvdf
  • Rnai
  • Ventricular Septum Malformations
  • Pax-8
ispartof: International Journal of Cardiology, 12 January 2012, Vol.154(1), pp.43-51
description: Cardiac-specific deletion of ALK3 is lethal in mid-gestation with ventricular septum malformations (VSM). This study was designed to define the Pax-8's role in heart development and cardiomyocyte apoptosis. Pathologic changes in the hearts of Pax-8 or ALK3 knockout and wild type control mice were determined by light and electron microscopy. Analysis of cardiomyocyte apoptosis was performed by TUNEL. The effect of Pax-8 gene deficiency on caspase-3 activity was examined after transfecting Pax-8 siRNA into cultured myoblast cell line. Mice with ALK3 or Pax-8 gene knockout but not wild type control animals showed the development of VSM. Increased cardiomyocyte apoptosis was found in homozygotes. Echocardiography showed that Pax-8 homozygote mice developed malfunction of the heart. Furthermore, the caspase-3 activity was significantly higher in the cells treated with Pax-8 siRNA as compared to those treated with negative control siRNA in H9C2...
language: eng
source:
identifier: ISSN: 0167-5273 ; E-ISSN: 1874-1754 ; DOI: 10.1016/j.ijcard.2010.08.057
fulltext: fulltext
issn:
  • 0167-5273
  • 01675273
  • 1874-1754
  • 18741754
url: Link


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titleThe defects in development and apoptosis of cardiomyocytes in mice lacking the transcriptional factor Pax-8
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subjectVentricular Septum Malformations ; Pax-8 ; Gene ; Bone Morphogenetic Protein Receptor ; Vsm ; Bmp ; Bmpr ; Alk3 ; Pax-8 ; Tunel ; Tgfβ ; Dab ; Pfa ; Hrp ; Ubm ; Pvdf ; Rnai ; Ventricular Septum Malformations ; Pax-8
descriptionCardiac-specific deletion of ALK3 is lethal in mid-gestation with ventricular septum malformations (VSM). This study was designed to define the Pax-8's role in heart development and cardiomyocyte apoptosis. Pathologic changes in the hearts of Pax-8 or ALK3 knockout and wild type control mice were determined by light and electron microscopy. Analysis of cardiomyocyte apoptosis was performed by TUNEL. The effect of Pax-8 gene deficiency on caspase-3 activity was examined after transfecting Pax-8 siRNA into cultured myoblast cell line. Mice with ALK3 or Pax-8 gene knockout but not wild type control animals showed the development of VSM. Increased cardiomyocyte apoptosis was found in homozygotes. Echocardiography showed that Pax-8 homozygote mice developed malfunction of the heart. Furthermore, the caspase-3 activity was significantly higher in the cells treated with Pax-8 siRNA as compared to those treated with negative control siRNA in H9C2...
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titleThe defects in development and apoptosis of cardiomyocytes in mice lacking the transcriptional factor Pax-8
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Cardiac-specific deletion of ALK3 is lethal in mid-gestation with ventricular septum malformations (VSM). This study was designed to define the Pax-8's role in heart development and cardiomyocyte apoptosis.

Pathologic changes in the hearts of Pax-8 or ALK3 knockout and wild type control mice were determined by light and electron microscopy. Analysis of cardiomyocyte apoptosis was performed by TUNEL. The effect of Pax-8 gene deficiency on caspase-3 activity was examined after transfecting Pax-8 siRNA into cultured myoblast cell line.

Mice with ALK3 or Pax-8 gene knockout but not wild type control animals showed the development of VSM. Increased cardiomyocyte apoptosis was found in homozygotes. Echocardiography showed that Pax-8 homozygote mice developed malfunction of the heart. Furthermore, the caspase-3 activity was significantly higher in the cells treated with Pax-8 siRNA as compared to those treated with negative control siRNA in H9C2...

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abstract

Cardiac-specific deletion of ALK3 is lethal in mid-gestation with ventricular septum malformations (VSM). This study was designed to define the Pax-8's role in heart development and cardiomyocyte apoptosis.

Pathologic changes in the hearts of Pax-8 or ALK3 knockout and wild type control mice were determined by light and electron microscopy. Analysis of cardiomyocyte apoptosis was performed by TUNEL. The effect of Pax-8 gene deficiency on caspase-3 activity was examined after transfecting Pax-8 siRNA into cultured myoblast cell line.

Mice with ALK3 or Pax-8 gene knockout but not wild type control animals showed the development of VSM. Increased cardiomyocyte apoptosis was found in homozygotes. Echocardiography showed that Pax-8 homozygote mice developed malfunction of the heart. Furthermore, the caspase-3 activity was significantly higher in the cells treated with Pax-8 siRNA as compared to those treated with negative control siRNA in H9C2...

pubElsevier Ireland Ltd
doi10.1016/j.ijcard.2010.08.057
lad01International Journal of Cardiology
date2012-01-12