ArticleBMC developmental biology2006
Ultrastructural analysis of development of myocardium in calreticulin-deficient mice.
Article in BMC developmental biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Deletion of the Wilms' Tumor Suppressor Gene in the Cardiac Troponin-T Lineage Reveals Novel Functions of WT1 in Heart Development.Frontiers in cell and developmental biology · 2021Article
- Energetic Interactions Between Subcellular Organelles in Striated Muscles.Frontiers in cell and developmental biology · 2020Review
- Maturation of Cardiac Energy Metabolism During Perinatal Development.Frontiers in physiology · 2018Review
- The functional diversity of essential genes required for mammalian cardiac development.Genesis (New York, N.Y. : 2000) · 2014Review
- Altered gene and protein expression in liver of the obese spontaneously hypertensive/NDmcr-cp rat.Nutrition & metabolism · 2012Article
- Article
- Decoded calreticulin-deficient embryonic stem cell transcriptome resolves latent cardiophenotype.Stem cells (Dayton, Ohio) · 2010Article
- Calnexin deficiency leads to dysmyelination.The Journal of biological chemistry · 2010Article
- ERp57 modulates STAT3 signaling from the lumen of the endoplasmic reticulum.The Journal of biological chemistry · 2010Article
- Thyroid hormone receptor alpha1 follows a cooperative CRM1/calreticulin-mediated nuclear export pathway.The Journal of biological chemistry · 2008Article
- Expression of endoplasmic reticulum chaperones in cardiac development.The open cardiovascular medicine journal · 2008Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCalreticulin is a Ca2+ binding chaperone of the endoplasmic reticulum which influences gene expression and cell adhesion. The levels of both vinculin and N-cadherin are induced by calreticulin expression, which play important roles in cell adhesiveness. Cardiac development is strictly dependent upon the ability of cells to adhere to their substratum and to communicate with their neighbours.
resultsWe show here that the levels of N-cadherin are downregulated in calreticulin-deficient mouse embryonic hearts, which may lead to the disarray and wavy appearance of myofibrils in these mice, which we detected at all investigated stages of cardiac development. Calreticulin wild type mice exhibited straight, thick and abundant myofibrils, which were in stark contrast to the thin, less numerous, disorganized myofibrils of the calreticulin-deficient hearts. Interestingly, these major differences were only detected in the developing ventricles while the atria of both calreticulin phenotypes were similar in appearance at all developmental stages. Glycogen also accumulated in the ventricles of calreticulin-deficient mice, indicating an abnormality in cardiomyocyte metabolism.
conclusionCalreticulin is temporarily expressed during heart development where it is required for proper myofibrillogenesis. We postulate that calreticulin be considered as a novel cardiac fetal gene.
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