The AKT/FOXO3A/Atrogin - 1 signaling pathways underlying cardiac regression after detraining in a mouse heart
| dc.contributor.committeeMember | Chung, Eunhee | |
| dc.contributor.committeeMember | Park, Yoonjung | |
| dc.contributor.committeeMember | Gonzales, Joaquin U. | |
| dc.creator | Lee, Wanseok | |
| dc.date.available | 2014-01-13T22:40:36Z | |
| dc.date.issued | 2013-12 | |
| dc.description.abstract | Exercise-induced cardiac hypertrophy reverses after cessation of exercise training. The Akt/FoxO3a/Atrogin-1 pathways have been implicated as important players in skeletal and cardiac muscle atrophy. However, little is known about the role of these pathways in cardiac muscle regression after exercise cessation. Thus, the purpose of this study was to determine the activities of Akt, FoxO, and to measure the levels of the muscle-specific E3 ligase, Atrogin-1 in cardiac muscle which has undergone regression of mass after cessation of exercise training. Three to four month old male C57Bl/6 mice were randomly divided into six groups: sedentary controls, 21 days of exercise, and 4 different time points of detraining after 21 days of voluntary wheel running (ie. 3 days, 5 days, 14 days, and 21 days). Body weight was not significantly different among groups. Exercise training significantly increased the heart weight/body weight ratio compared to sedentary controls (13% increase in HW/BW), but this growth was regressed after 21 days of detraining. We found that phosphorylation of Akt normalized to total Akt was significantly increased in the exercise group, and also in the 3-, 5-, and 14 days of detraining groups, but was significantly decreased in the 21 days of detraining group compared to the sedentary control group. However, the phospho-FoxO3a to total FoxO3a ratio was not different among groups. Interestingly, the level of Atrogin-1 was significantly decreased in 14-, and 21 days of detraining groups. Our results suggest that cardiac regression following exercise cessation is not mediated by up-regulation of Atrogin-1. Taken together, this study demonstrates that cardiac regression occurs after 21 days of exercise cessation and it may be partially mediated by inactivation of Akt. | |
| dc.format.mimetype | application/pdf | |
| dc.identifier.uri | http://hdl.handle.net/2346/58225 | |
| dc.language.iso | eng | |
| dc.rights.availability | Unrestricted. | |
| dc.subject | Heart--Diseases--Patients--Rehabilitation | |
| dc.subject | Heart | |
| dc.title | The AKT/FOXO3A/Atrogin - 1 signaling pathways underlying cardiac regression after detraining in a mouse heart | |
| dc.type | Thesis | |
| thesis.degree.department | Health Exercise and Sport Sciences | |
| thesis.degree.discipline | Exercise and Sport Sciences | |
| thesis.degree.grantor | Texas Tech University | |
| thesis.degree.level | Masters | |
| thesis.degree.name | Master of Science |
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