Key result
Hepatic vitamin A depletion reduces post-MI ventricular remodeling and expands cardiac progenitor cells in mice.
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Shows depletion of hepatic vitamin A stores alters ventricular gene expression and progenitor cells in mice, suggesting modified injury response.
To determine whether hepatic depletion of vitamin A (VA) stores has an effect on the postnatal heart, studies were carried out with mice lacking liver retinyl ester stores fed either a VA-sufficient (LRVAS) or VA-deficient (LRVAD) diet (to deplete circulating retinol and extrahepatic stores of retinyl esters). There were no observable differences in the weights or gross morphology of hearts from LRVAS or LRVAD mice relative to sex-matched, age-matched, and genetically matched wild-type (WT) controls fed the VAS diet (WTVAS), but changes in the transcription of functionally relevant genes were consistent with a state of VAD in LRVAS and LRVAD ventricles. In silico analysis revealed that 58/67 differentially expressed transcripts identified in a microarray screen are products of genes that have DNA retinoic acid response elements. Flow cytometric analysis revealed a significant and cell-specific increase in the number of proliferating Sca-1 cardiac progenitor cells in LRVAS animals relative to WTVAS controls. Before myocardial infarction, LRVAS and WTVAS mice had similar cardiac systolic function and structure, as measured by echocardiography, but, unexpectedly, repeat echocardiography demonstrated that LRVAS mice had less adverse remodeling by 1 wk after myocardial infarction. Overall, the results demonstrate that the adult heart is responsive to retinoids, and, most notably, reducing hepatic VA stores (while maintaining circulating levels of VA) impacts ventricular gene expression profiles, progenitor cell numbers, and response to injury.
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Asson–Batres et al. (2016) studied Vitamin A deficiency and myocardial infarction (postnatal mouse heart). Hepatic retinyl ester store depletion with vitamin A-sufficient (LRVAS) or vitamin A-deficient (LRVAD) diet vs. Wild-type controls fed a vitamin A-sufficient diet (WTVAS) was evaluated on Ventricular gene expression, Sca-1 cardiac progenitor cell proliferation, and post-myocardial infarction cardiac remodeling. Hepatic vitamin A depletion in mice altered ventricular gene expression (58/67 transcripts with retinoic acid response elements), increased Sca-1+ progenitor cells, and reduced remodeling 1 wk post-MI.
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