Nizami 2024 Abstract IOC163

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Nizami HL, Szybowska P, Singhal P, Lee CF (2024) Investigating the effect of Nampt overexpression on cardiac mitochondrial respiration in Ndufs4-cKO mice. Mitochondr Physiol Network 28.11.

Link: IOC163

Nizami Hina Lateef, Szybowska Patrycja, Singhal Pratyaksh, Lee Chi Fung (2024)

Event: IOC163

NAD+ decline and redox imbalance have been reported in different cardiometabolic diseases. We have earlier shown that cardiomyocyte-specific deletion of Ndufs4 (NADH:ubiquinone oxidoreductase subunit S4), a protein critical for Complex I assembly in the mitochondrial electron transport system, induces NAD+ redox imbalance and exacerbates diabetic cardiomyopathy in mice. We have also reported reduction of Complex I-driven State 3 respiration in permeabilized cardiac fibers from these mice. However, it is not known whether cardiac-specific overexpression of Nampt (nicotinamide phosphoribosyltranferase), the rate-limiting enzyme of NAD+ biosynthesis through salvage pathway, can rescue the decline of Complex I-driven respiration in these Ndufs4-cKO hearts.

Hearts were harvested from Ndufs4-flox/flox (Control) and cardiac-specific Ndufs4-knockout (cKO) mice and mitochondria were isolated. Oroboros O2k fluorespirometer was used to measure mitochondrial oxygen consumption rate. To each chamber, 50 Β΅g mitochondria were loaded, followed by addition of pyruvate, malate and ADP to study Complex I-driven respiration, and succinate and ADP to measure Complex II-driven respiration, respectively. Mitochondria from the cKO showed 39.7Β±2.26% decline in Complex I-driven State 3 respiration, whereas no significant change was observed in Complex II-driven respiration. We are currently using the O2k to compare the mitochondrial respiration in Ndufs4-cKO mouse hearts with and without cardiac-specific Nampt overexpression.


β€’ Bioblast editor: Plangger M


Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Cardiovascular, Myopathy 

Organism: Mouse  Tissue;cell: Heart  Preparation: Isolated mitochondria 


Coupling state: OXPHOS  Pathway: N, S  HRR: Oxygraph-2k 


Affiliations

Nizami Hina Lateef1, Szybowska Patrycja1,2, Singhal Pratyaksh1, Lee Chi Fung1,2,3
  1. Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
  2. Department of Biochemistry and Molecular Biology;
  3. Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK.
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