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Updated: Jun 28, 2026
08:57
En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
Published on: July 27, 2022
Expression of endoplasmic reticulum chaperones in cardiac development
Sylvia Papp1, Xiaochu Zhang, Eva Szabo
1Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
The Open Cardiovascular Medicine Journal
|October 25, 2008
Summary
During embryonic development, cardiac protein synthesis does not induce endoplasmic reticulum stress despite high chaperone levels. Adult hearts show less protein synthesis but higher endoplasmic reticulum stress markers, suggesting distinct stress responses.
Area of Science:
- Cardiovascular Biology
- Cellular Stress Response
- Developmental Biology
Background:
- Cardiac pathologies often activate the fetal gene program.
- The relationship between fetal gene program activation and endoplasmic reticulum stress during development is unclear.
Purpose of the Study:
- To investigate whether cardiogenesis (heart development) induces endoplasmic reticulum (ER) stress.
- To determine if activation of the fetal gene program during cardiac development causes ER stress.
Main Methods:
- Examined chaperone protein expression in embryonic versus adult hearts.
- Investigated endoplasmic reticulum stress pathways, including ATF6alpha and caspase levels, during cardiogenesis.
Main Results:
- Stress-related chaperones were more abundant in embryonic hearts, indicating ER stress during normal cardiac development.
- Adult hearts showed higher levels of ATF6alpha, caspase 7, and caspase 12.
- Embryonic development involves high protein synthesis but no significant ER stress, unlike postnatal remodeling.
Conclusions:
- Endoplasmic reticulum stress is present during normal embryonic cardiac development.
- Despite high protein synthesis load in embryonic hearts, it does not induce apoptosis-associated ER stress.
- Adult hearts exhibit increased ER stress markers, suggesting different stress dynamics post-development.
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