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dc.contributor.advisorGregorio, Carolen
dc.contributor.authorPatel, Parth Mahendra
dc.creatorPatel, Parth Mahendraen
dc.date.accessioned2017-08-08T17:19:20Z
dc.date.available2017-08-08T17:19:20Z
dc.date.issued2017
dc.identifier.urihttp://hdl.handle.net/10150/625115
dc.description.abstractRationale: Cardiac hypertrophy is the enlargement of the heart and can be induced by pathological and non-pathological events. The Fragile X family of RNA-binding proteins have been shown to be involved in cardiac structure and development (Mientjes et al, 2004) (Padje et al, 2009). Potential links between FXR1 and hypertrophy have not been significantly studied. Objective: To study the effect that varying expression of FXR1 has upon hypertrophy, and the molecular role FXR1 plays in hypertrophy. Method and Results: Following a voluntary running protocol, FXR1 wild-type mice had significant cardiac hypertrophy while FXR1 heterozygous mice (reduced FXR1 expression) had a blunted response with no significant hypertrophy. Cardiomyocyte size analysis showed that FXR1 overexpression (~9-fold increase) caused significant size reduction and FXR1 knockdown caused significant size increase. RNA immunoprecipitation showed multiple components of the PI3K/AKT/mTOR pathway associating with FXR1 in a protein/RNA complex. Western blotting showed that exercised FXR1 heterozygous mice had an increased expression of phosphorylated AKT versus non-exercised wild-type mice. Varying FXR1 expression in cells did not affect p-AKT expression. Conclusions: The amount of FXR1 in mice and cells appears to alter the severity of cardiac hypertrophy. FXR1 may regulate cardiac hypertrophy, but how this occurs is still unclear.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.titleDeciphering the Role of FXR1 in Cardiac Hypertrophyen_US
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.levelbachelorsen
thesis.degree.disciplineHonors Collegeen
thesis.degree.disciplineMolecular and Cellular Biologyen
thesis.degree.nameB.S.en
refterms.dateFOA2018-04-25T20:04:16Z
html.description.abstractRationale: Cardiac hypertrophy is the enlargement of the heart and can be induced by pathological and non-pathological events. The Fragile X family of RNA-binding proteins have been shown to be involved in cardiac structure and development (Mientjes et al, 2004) (Padje et al, 2009). Potential links between FXR1 and hypertrophy have not been significantly studied. Objective: To study the effect that varying expression of FXR1 has upon hypertrophy, and the molecular role FXR1 plays in hypertrophy. Method and Results: Following a voluntary running protocol, FXR1 wild-type mice had significant cardiac hypertrophy while FXR1 heterozygous mice (reduced FXR1 expression) had a blunted response with no significant hypertrophy. Cardiomyocyte size analysis showed that FXR1 overexpression (~9-fold increase) caused significant size reduction and FXR1 knockdown caused significant size increase. RNA immunoprecipitation showed multiple components of the PI3K/AKT/mTOR pathway associating with FXR1 in a protein/RNA complex. Western blotting showed that exercised FXR1 heterozygous mice had an increased expression of phosphorylated AKT versus non-exercised wild-type mice. Varying FXR1 expression in cells did not affect p-AKT expression. Conclusions: The amount of FXR1 in mice and cells appears to alter the severity of cardiac hypertrophy. FXR1 may regulate cardiac hypertrophy, but how this occurs is still unclear.


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