ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Systolic dysfunction in cardiac-specific ligand-inducible MerCreMer transgenic mice.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 70 citations in OpenAlex.
- Cardiomyocyte cytosolic nuclear self-DNA contributes to the pathogenesis of desmoplakin cardiomyopathy.JCI insight · 2025Article
- Depletion of Mitochondrial Cyclophilin D in Endothelial and Smooth Muscle Cells Attenuates Vascular Dysfunction and Hypertension.Function (Oxford, England) · 2025Article
- Cre recombinase affects calcium dynamics already in young mice.Frontiers in pharmacology · 2025Article
- Prolonged tamoxifen-enriched diet is associated with cardiomyopathy and nutritional frailty in mice.Experimental physiology · 2024Article
- α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor.EMBO reports · 2024Article
- Myosin Light Chain Phosphatase Plays an Important Role in Cardiac Fibrosis in a Model of Mineralocorticoid Receptor-Associated Hypertension.Journal of the American Heart Association · 2024Article
- Review
- Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis.International journal of molecular sciences · 2023Article
- PANoptosis is a prominent feature of desmoplakin cardiomyopathy.The journal of cardiovascular aging · 2023Article
- Postnatal Deletion of Bmal1 in Cardiomyocyte Promotes Pressure Overload Induced Cardiac Remodeling in Mice.Journal of the American Heart Association · 2022Article
- Measuring cardiomyocyte cell-cycle activity and proliferation in the age of heart regeneration.American journal of physiology. Heart and circulatory physiology · 2022Review
- Timing of food intake in mice unmasks a role for the cardiomyocyte circadian clock mechanism in limiting QT-interval prolongation.Chronobiology international · 2022Article
- Myeloid hypoxia-inducible factor HIF1A provides cardio-protection during ischemia and reperfusionFrontiers in cardiovascular medicine · 2022Article
- Ablation of cardiomyocyte-derived BDNF during development causes myocardial degeneration and heart failure in the adult mouse heart.Frontiers in cardiovascular medicine · 2022Article
- Optimization of tamoxifen-induced gene regulation in cardiovascular research.The journal of cardiovascular aging · 2022Article
- Effects of tamoxifen inducible MerCreMer on gene expression in cardiac myocytes in mice.The journal of cardiovascular aging · 2022Article
- Generation and characterization of a Myh6-driven Cre knockin mouse line.Transgenic research · 2021Article
- 4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice.Basic research in cardiology · 2021Article
- Cardiomyocyte Deletion ofFrontiers in physiology · 2021Article
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The Cre-loxP system is a useful tool to study the physiological effects of gene knockout in the heart. One limitation with using this system in the heart is the toxic effect of chronic expression of the Cre recombinase. To circumvent this limitation, a widely used inducible cardiac-specific model, Myh6-MerCreMer (Cre), using tamoxifen (TAM) to activate Cre has been developed. The current study examined cardiac function in Cre-positive C57B/J6 mice exposed to one, three, or five daily doses of a 40 mg/kg TAM to induce Cre activity specifically in the heart. Echocardiography demonstrated no statistically significant differences in systolic function (SF) at baseline as assessed by fractional shortening. In mice exposed to five injections, a significant fall in all determinants of SF was observed 6 days after TAM was initiated. However, SF returned to baseline levels 10 days after TAM initiation although the hearts exhibited significant hypertrophy. Heart weight-to-tibia length ratios were 73 ± 3, 78.5 ± 6, and 87.6 ± 9 mg/cm for one, three, and five TAM injections, respectively. TAM had no effect on cardiac function or hypertrophy in Cre-negative mice. Cre-positive mice receiving five TAM injections had significant reductions in cardiac mitochondrial ATP and significant reductions in the expression of proteins important for the regulation of cardiac oxidative phosphorylation including peroxisome proliferator-activated receptor-γ coactivator-1α and pyruvate dehydrogenase kinase-4. Thus inducible cardiac-specific activation of Cre recombinase caused a transient decline in SF that was dependent on the number of TAM doses and associated with significant hypertrophy and alterations in mitochondrial ATP and important proteins involved in the regulation of cardiac oxidative phosphorylation.
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