Related Experiment Video
Updated: Jun 22, 2026
07:14
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
Mitochondrial OPA1, apoptosis, and heart failure.
Le Chen1, Qizhi Gong, James P Stice
1Molecular and Cellular Cardiology, Department of Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA.
Cardiovascular Research
|June 5, 2009
Summary
Mitochondrial fusion protein OPA1 (optic atrophy 1) decreases in heart failure, leading to small, dysfunctional mitochondria and increased cell death. This contributes to progressive heart dysfunction.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Dynamics
- Cellular Pathophysiology
Background:
- Mitochondrial fusion and fission are critical for maintaining normal mitochondrial function.
- Mitochondria in heart failure (HF) are often small and dysfunctional.
- Fusion proteins were hypothesized to be reduced in HF.
Purpose of the Study:
- To investigate the role of mitochondrial fusion proteins in heart failure.
- To determine if optic atrophy 1 (OPA1) expression is altered in HF.
- To understand the functional consequences of altered OPA1 in cardiac cells.
Main Methods:
- Western blotting to assess OPA1 protein levels in human and rat HF.
- Confocal and electron microscopy to examine mitochondrial morphology.
- Simulated ischemia and OPA1 knockdown/overexpression in H9c2 cells.
Main Results:
- OPA1 protein expression was decreased in failing hearts.
- Mitochondria in HF were small and fragmented, correlating with reduced OPA1.
- OPA1 reduction increased apoptosis and mitochondrial fragmentation; overexpression did not prevent ischemia-induced apoptosis.
- Both OPA1 reduction and overexpression increased cytochrome c release.
Conclusions:
- This study is the first to report changes in mitochondrial fusion/fission proteins in cardiovascular disease.
- Altered OPA1 impacts mitochondrial function and apoptosis in HF.
- These changes contribute to cardiomyocyte loss and disease progression in the failing heart.
More Related Videos
09:40Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
Published on: January 19, 2017
11:26Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer
Published on: February 13, 2019
Related Concept Videos
01:17Pathophysiology of Heart Failure
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
01:29Heart Failure II: Pathophysiology
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
01:27Heart Failure I: Introduction
Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
01:37Mitochondria
Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
01:31The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
01:45Mitochondrial Membranes
A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...