RESEARCH ARTICLE


Expression of Endoplasmic Reticulum Chaperones in Cardiac Development



Sylvia Papp1, Xiaochu Zhang1, Eva Szabo1, Marek Michalak2, Michal Opas*, 1
1 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
2 Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada


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© Papp et al.; Licensee Bentham Open

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

* Address correspondence to this author at the Department of Laboratory Medicine and Pathobiology, University of Toronto, 1 King's College Circle, Medical Sciences Building, room 6326, Toronto, Ontario, M5S 1A8 Canada; Tel: (416) 978-8947, (416) 971-2140; Fax: (416) 978-5959; E-mail: m.opas@utoronto.ca


Abstract

To determine if cardiogenesis causes endoplasmic reticulum stress, we examined chaperone expression. Many cardiac pathologies cause activation of the fetal gene program, and we asked the reverse: could activation of the fetal gene program during development induce endoplasmic reticulum stress/chaperones?

We found stress related chaperones were more abundant in embryonic compared to adult hearts, indicating endoplasmic reticulum stress during normal cardiac development. To determine the degree of stress, we investigated endoplasmic reticulum stress pathways during cardiogenesis. We detected higher levels of ATF6α, caspase 7 and 12 in adult hearts. Thus, during embryonic development, there is large protein synthetic load but there is no endoplasmic reticulum stress. In adult hearts, chaperones are less abundant but there are increased levels of ATF6α and ER stress-activated caspases. Thus, protein synthesis during embryonic development does not seem to be as intense a stress as is required for apoptosis that is found during postnatal remodelling.

Keywords: Heart, endoplasmic reticulum stress, chaperones, unfolded protein response, embryonic development, apoptosis.