Characterization of mediators of cardiac and renal development in response to increased prenatal testosterone
dc.contributor.author | Maresh, Ryan W., author | |
dc.contributor.author | Anthony, Russell, advisor | |
dc.date.accessioned | 2024-03-13T20:12:25Z | |
dc.date.available | 2024-03-13T20:12:25Z | |
dc.date.issued | 2008 | |
dc.description.abstract | Previously reported differences in cardiac and kidney weights of offspring from ewes prenatally treated with testosterone suggested the development of systemic hypertension. To determine if prenatal androgen excess influences the expression of key mediators, angiopoietin 1 (Ang1), angiopoietin 2 (Ang2), tunica interna endothelial cell kinase-2 (Tie2), angiotensin II receptor subtypes 1 and 2 (AT1 and AT2), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), VEGF receptor 1 (VEGF R1), VEGF receptor 2 (VEGF R2), insulin receptor β (IRβ), glucose transporter 1 (GLUT1), and glucose transporter 4 (GLUT4) were evaluated from fetal hearts, fetal kidney, left ventricle (LV), right ventricle (RV), and kidney. We hypothesized that mRNA and protein concentrations were altered and that the changes persist into adulthood. At fetal Day 90 a significant increase (p = 0.021) in IRβ mRNA concentration of was seen in the heart, whereas VEGF mRNA concentration was significantly reduced (p = 0.044) in the kidney. In 9 month RV, eNOS mRNA concentration was significantly reduced in the treatment group (p = 0.019). In the 9 month kidney, significant increases in GLUT4 mRNA concentration (p = 0.047) and eNOS protein concentration (p = 0.027) were seen in the treatment group. At 21 months of age, Ang1 mRNA concentration in the treatment group was significantly reduced (p = 0.025) in the LV. AT1 mRNA concentration was significantly decreased (p = 0.004) in the RV of the treatment group. LV eNOS concentration was significantly reduced (p = 0.032), while RV eNOS mRNA concentration was significantly decreased (p < 0.001) in the treatment group. Significant decreases in GLUT1 mRNA concentration were detected in the LV (p = 0.013) and RV (p = 0.006), and RV GLUT4 mRNA concentration was significantly decreased (p = 0.003) in the treatment group. LV IRβ concentration was significantly reduced (p = 0.036) in the treatment group. In the kidney, VEGF R2 mRNA concentration was significantly reduced (p = 0.024) in the treatment group. Taken together, the data supports the development of systemic hypertension and insulin resistance with age following prenatal androgen exposure. | |
dc.format.medium | born digital | |
dc.format.medium | doctoral dissertations | |
dc.identifier | ETDF_Maresh_2008_3332712.pdf | |
dc.identifier.uri | https://hdl.handle.net/10217/237861 | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | Colorado State University. Libraries | |
dc.relation.ispartof | 2000-2019 | |
dc.rights | Copyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright. | |
dc.rights.license | Per the terms of a contractual agreement, all use of this item is limited to the non-commercial use of Colorado State University and its authorized users. | |
dc.subject | androgen excess | |
dc.subject | fetal programming | |
dc.subject | metabolic regulation | |
dc.subject | prenatal | |
dc.subject | renal development | |
dc.subject | testosterone | |
dc.subject | physiology | |
dc.title | Characterization of mediators of cardiac and renal development in response to increased prenatal testosterone | |
dc.type | Text | |
dcterms.rights.dpla | This Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). | |
thesis.degree.discipline | Biomedical Sciences | |
thesis.degree.grantor | Colorado State University | |
thesis.degree.level | Doctoral | |
thesis.degree.name | Doctor of Philosophy (Ph.D.) |
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