Retinoid Regulated Gene Expression in the Heart

Document Type

Event

Faculty Mentor

Ian Gans

Abstract

Vitamin A stores are mobilized following myocardial infarction, and Vitamin A metabolism concurrently increases in the heart. Previous studies have demonstrated that Vitamin A (retinol) and its active metabolites (retinoids) influence injury response, pathological remodeling, and heart failure. Our lab has found that Vitamin A deficiency impairs heart contractility, although the underlying mechanisms remain unclear. Given that retinoids regulate gene expression, the present study examined the expression of genes of interest in hearts from Vitamin A-deficient and Vitamin A-sufficient mice. Quantitative real-time PCR (qRT-PCR) was used to assess the expression of several genes involved in contractile and metabolic processes, previously identified as potential retinoid targets. The results did not confirm these previously suggested targets, indicating that further investigation is required to elucidate the mechanisms of retinoid action during heart injury.

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Retinoid Regulated Gene Expression in the Heart

Vitamin A stores are mobilized following myocardial infarction, and Vitamin A metabolism concurrently increases in the heart. Previous studies have demonstrated that Vitamin A (retinol) and its active metabolites (retinoids) influence injury response, pathological remodeling, and heart failure. Our lab has found that Vitamin A deficiency impairs heart contractility, although the underlying mechanisms remain unclear. Given that retinoids regulate gene expression, the present study examined the expression of genes of interest in hearts from Vitamin A-deficient and Vitamin A-sufficient mice. Quantitative real-time PCR (qRT-PCR) was used to assess the expression of several genes involved in contractile and metabolic processes, previously identified as potential retinoid targets. The results did not confirm these previously suggested targets, indicating that further investigation is required to elucidate the mechanisms of retinoid action during heart injury.

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