Expression and function of transcription factor Mox-1 during early heart valve development

Persistent Link:
http://hdl.handle.net/10150/284125
Title:
Expression and function of transcription factor Mox-1 during early heart valve development
Author:
Wendler, Christopher Charles
Issue Date:
2000
Publisher:
The University of Arizona.
Rights:
Copyright © 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.
Abstract:
Epithelial to mesenchymal cell transformation (EMT) in the atrioventricular canal (AV canal) produces a population of fibroblast cells that contribute to the mitral and tricuspid valves of the fully formed heart. Formation of these cells is critical for normal heart development and disruption of this process leads to congenital heart disease. This study describes the role of the homeodomain containing transcription factor Mox-1 during this cell transformation process. Mox-1 protein and mRNA expression were detected during cell transformation in the cardiac cushions. This expression corresponded in time to stages of EMT characterized by cell shape change and invasion of the extracellular matrix. Antisense oligonucleotides to Mox-1 inhibited cell transformation in cultured AV canal explants. Previous reports indicated that the TGFβ3 signaling pathway also regulates cell transformation at similar stages. Experiments inhibiting the TGFβ3 pathway also inhibit Mox-1 expression. A 2kb portion of the Mox-1 promoter was cloned and a portion of this construct demonstrated a capacity to initiate transcription in AV canal cultures. The active fragment of the Mox-1 promoter was responsive to TGFβ3 signaling. This study indicates that Mox-1 is necessary but not sufficient for cell transformation in the AV canal cushions and is regulated by an important signaling pathway involved in this process.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Biology, Cell.; Health Sciences, Human Development.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Cell Biology and Anatomy
Degree Grantor:
University of Arizona
Advisor:
Runyan, Raymond B.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleExpression and function of transcription factor Mox-1 during early heart valve developmenten_US
dc.creatorWendler, Christopher Charlesen_US
dc.contributor.authorWendler, Christopher Charlesen_US
dc.date.issued2000en_US
dc.publisherThe University of Arizona.en_US
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_US
dc.description.abstractEpithelial to mesenchymal cell transformation (EMT) in the atrioventricular canal (AV canal) produces a population of fibroblast cells that contribute to the mitral and tricuspid valves of the fully formed heart. Formation of these cells is critical for normal heart development and disruption of this process leads to congenital heart disease. This study describes the role of the homeodomain containing transcription factor Mox-1 during this cell transformation process. Mox-1 protein and mRNA expression were detected during cell transformation in the cardiac cushions. This expression corresponded in time to stages of EMT characterized by cell shape change and invasion of the extracellular matrix. Antisense oligonucleotides to Mox-1 inhibited cell transformation in cultured AV canal explants. Previous reports indicated that the TGFβ3 signaling pathway also regulates cell transformation at similar stages. Experiments inhibiting the TGFβ3 pathway also inhibit Mox-1 expression. A 2kb portion of the Mox-1 promoter was cloned and a portion of this construct demonstrated a capacity to initiate transcription in AV canal cultures. The active fragment of the Mox-1 promoter was responsive to TGFβ3 signaling. This study indicates that Mox-1 is necessary but not sufficient for cell transformation in the AV canal cushions and is regulated by an important signaling pathway involved in this process.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectBiology, Cell.en_US
dc.subjectHealth Sciences, Human Development.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineCell Biology and Anatomyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorRunyan, Raymond B.en_US
dc.identifier.proquest9965925en_US
dc.identifier.bibrecord.b40485535en_US
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