Open Access. Powered by Scholars. Published by Universities.®
Biochemistry, Biophysics, and Structural Biology Commons™
Open Access. Powered by Scholars. Published by Universities.®
- Discipline
Articles 1 - 4 of 4
Full-Text Articles in Biochemistry, Biophysics, and Structural Biology
Modulation Of Electron Transport By Metformin In Cardiac Protection: Role Of Complex I, Ahmed Abdul Hussein Mohsin
Modulation Of Electron Transport By Metformin In Cardiac Protection: Role Of Complex I, Ahmed Abdul Hussein Mohsin
Theses and Dissertations
Modulation of mitochondrial complex I during reperfusion reduces cardiac injury. Complex I exists in two structural states: active (A) and deactive (D) with transition from A→D during ischemia. Reperfusion reactivates D→A with an increase in ROS production. Metformin preserves the D-Form. Our aim was to study the contribution of maintenance of deactivation of complex I during early reperfusion by metformin to protect against ischemia reperfusion injury. Our results showed that metformin decreased H9c2 cardiomyoblast apoptosis and total cell death following simulated ischemia for six hours followed by reoxygenation for twenty four hours compared to untreated cells. Reactive oxygen species (ROS) …
A Mechanistic Study Of An Ipsc Model For Leigh’S Disease Caused By Mtdna Mutataion (8993 T>G), John P. Galdun
A Mechanistic Study Of An Ipsc Model For Leigh’S Disease Caused By Mtdna Mutataion (8993 T>G), John P. Galdun
Theses and Dissertations
Mitochondrial diseases encompass a broad range of devastating disorders that typically affect tissues with high-energy requirements. These disorders have been difficult to diagnose and research because of the complexity of mitochondrial genetics, and the large variability seen among patient populations. We have devised and carried out a mechanistic study to generate a cell based model for Leigh’s disease caused by mitochondrial DNA mutation 8993 T>G. Leigh’s disease is a multi-organ system disorder that depends heavily on the mutation burden seen within various tissues. Using new reprogramming and sequencing technologies, we were able to show that Leigh’s disease patient fibroblasts …
Metabolic Remodeling And Mitochondrial Dysfunction In Maladaptive Right Ventricular Hypertrophy Secondary To Pulmonary Arterial Hypertension, Jose Gomez-Arroyo
Metabolic Remodeling And Mitochondrial Dysfunction In Maladaptive Right Ventricular Hypertrophy Secondary To Pulmonary Arterial Hypertension, Jose Gomez-Arroyo
Theses and Dissertations
Right ventricular dysfunction is the most frequent cause of death in patients with pulmonary arterial hypertension. Although abnormal energy substrate use has been implicated in the development of chronic left heart failure, data describing such metabolic remodeling in failing right ventricular tissue remain incomplete. In the present dissertation we sought to characterize metabolic gene expression changes and mitochondrial dysfunction in functional and dysfunctional RV hypertrophy. Two different rat models of RV hypertrophy were studied. The model of right ventricular failure (SU5416/hypoxia) exhibited a significantly decreased gene expression of peroxisome proliferator-activated receptor- coactivator-1α, peroxisome proliferator- activated receptor-α and estrogen-related receptor-α. The …
Non-Canonical Roles For Stat1 And Stat2 In Mitochondrial Biogenesis And Fasting Homeostasis., Jennifer Sisler
Non-Canonical Roles For Stat1 And Stat2 In Mitochondrial Biogenesis And Fasting Homeostasis., Jennifer Sisler
Theses and Dissertations
The signal transducer and activator of transcription 1 (STAT1) and 2 (STAT2) are primarily activated by interferons and play a central role in orchestrating responses to a variety of pathogens by activating the transcription of nuclear encoded genes that mediate antiviral, antigrowth and immune surveillance responses. In addition to their nuclear effects, we report that STAT1 and STAT2 inhibit the expression of mitochondrial encoded mRNAs by activating type I interferons (IFNβ) under basal conditions. STAT1-/- livers also exhibit elevated levels of nuclear encoded components of the electron transport chain (ETC). Treatment of wild-type mice with IFNβ inhibits both mitochondrial and …