Regulation by a developmental transcription factor of signaling enzymes related to atrial fibrillation Public

http://ir.library.oregonstate.edu/concern/honors_college_theses/sj139385w

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  • Atrial fibrillation is the most common cardiac arrhythmia, and the mechanisms that lead to this heart defect are not fully understood. Consequently, treatments for this defect do not currently reverse structural or molecular variations that lead to cardiac arrhythmia. Loss of the gene coding for the transcription factor Pitx2 leads to abnormal cardiogenesis, and as a result mice with Pitx2 mutations are models susceptible to atrial fibrillation. In both humans and mice, increased expression of the enzyme Phospholipase C beta (PLC-β) correlates with atrial remodeling, hypertrophy, and apoptosis. Pitx2 was hypothesized to suppress the expression of PLC-β, and the reduction of Pitx2 was hypothesized to up-regulate hypertrophic and apoptotic signaling pathways that typically accompany atrial fibrillation. To test these hypotheses PLC-β expression was measured in mice mutated to have no Pitx2 gene, and compared to PLC-β expression in normal mice. Expression of PLC-β was measured by isolating mRNA from the mouse atria, and performing quantitative real-time polymerase chain reaction (qRT-PCR) assays for PLC-β. Western blot assays were utilized to determine relative PLC-β protein levels after elevation of Pitx2 in cultured cardiomyoblast cells. The consequences of this research will be followed in adult mice to indicate mechanisms for congenital heart defects, prospectively identifying factors in increased susceptibility to atrial fibrillation, and impart to potential drug development.
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