Measurement of Mitochondrial Respiration and Motility in Acute Care

Jang, David H.; Greenwood, John C.; Spyres, Meghan B.; Eckmann, David M.

doi:10.1177/0885066616658449

Cited by 40 publications

(40 citation statements)

References 45 publications

(51 reference statements)

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“…The rate of mitochondrial oxygen consumption (OCR) can be measured using the XF Extracellular Flux Analyzer (Seahorse Bioscience), the Oroboros O2K or the Clark-type oxygen electrode ( 172 , 173 ). Seahorse XF Analyzers measure the concentration of dissolved oxygen and pH to quantify the oxygen consumption and extracellular acidification rate in the media in multi-well plates.…”

Section: Assessing Cell Metabolismmentioning

confidence: 99%

“…Four injection ports in each well allow for addition of reagents. However, the Seahorse requires cells to be adhered to the wells, multiple additions of substrates are not possible and the individual wells are not self-contained and thus cells can be affected by gases from adjacent wells ( 172 ). The Clark-type oxygen electrode is embedded in individual reaction chambers and cells are added in suspension in the respiration media ( 173 ).…”

Section: Assessing Cell Metabolismmentioning

confidence: 99%

“…Unlimited reagents and substrates can be added by manual addition. This system is more automated in the Oroboros O2K which also includes optical sensors to allow for detection of fluorescent dyes so that parameters such as ATP production or mitochondrial membrane potential may be measured ( 172 ).…”

Section: Assessing Cell Metabolismmentioning

confidence: 99%

See 2 more Smart Citations

Changing Metabolism in Differentiating Cardiac Progenitor Cells—Can Stem Cells Become Metabolically Flexible Cardiomyocytes?

Malandraki-Miller

Lopez

Al-Siddiqi

et al. 2018

Front. Cardiovasc. Med.

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The heart is a metabolic omnivore and the adult heart selects the substrate best suited for each circumstance, with fatty acid oxidation preferred in order to fulfill the high energy demand of the contracting myocardium. The fetal heart exists in an hypoxic environment and obtains the bulk of its energy via glycolysis. After birth, the “fetal switch” to oxidative metabolism of glucose and fatty acids has been linked to the loss of the regenerative phenotype. Various stem cell types have been used in differentiation studies, but most are cultured in high glucose media. This does not change in the majority of cardiac differentiation protocols. Despite the fact that metabolic state affects marker expression and cellular function and activity, the substrate composition is currently being overlooked. In this review we discuss changes in cardiac metabolism during development, the various protocols used to differentiate progenitor cells to cardiomyocytes, what is known about stem cell metabolism and how consideration of metabolism can contribute toward maturation of stem cell-derived cardiomyocytes.

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Section: Assessing Cell Metabolismmentioning

confidence: 99%

Section: Assessing Cell Metabolismmentioning

confidence: 99%

See 1 more Smart Citation

Changing Metabolism in Differentiating Cardiac Progenitor Cells—Can Stem Cells Become Metabolically Flexible Cardiomyocytes?

Malandraki-Miller

Lopez

Al-Siddiqi

et al. 2018

Front. Cardiovasc. Med.

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show abstract

“…The study of mitochondrial respiration has also extended to areas of acute care that include: sepsis, traumatic injuries, and toxicology. 10 Whole blood cells such as peripheral blood mononuclear cells (PBMCs) and platelets have been explored for their potential to act as sensitive biomarkers for mitochondrial dysfunction in lieu of invasive and time consuming tissue biopsies. 11,12 …”

Section: Introductionmentioning

confidence: 99%

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

Jang

Kelly

Hardy

et al. 2017

Clinical Toxicology

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Objectives Carbon monoxide (CO) is a colorless and odorless gas that is an important cause of poisoning mortality and morbidity in the United States. At this time there is no reliable method to predict severity of poisoning or clinical prognosis following CO exposure. Whole blood cells such as peripheral blood mononuclear cells (PBMCs) and platelets have been explored for their potential to act as sensitive biomarkers for mitochondrial dysfunction. Design The objective of this study was to measure mitochondrial respiration using intact cells obtained from patients exposed to CO as a potential biomarker for mitochondrial inhibition with results that can be obtained in a time frame useful for guiding clinical care. This was a prospective, observational pilot study performed from July 2015 to July 2016 at a single academic tertiary care center that is the location of the region’s only multi chamber hyperbaric. Measurements Clinical characteristics, patient demographics, mitochondrial respiration and outcomes were recorded. Main results There were 7 patients enrolled with a mean COHb level was (26.8+/−10) with a mean lactate of (1.1+/−0.4 mmol/L). All 7 CO exposures were related to heat generators used during winter months with two deaths. There was a positive correlation between maximal respiration and COHb levels with both a high maximal respiration and high spare respiratory capacity correlating with a high COHb level. There was a subset of PBMCs (n=4) that were analyzed for Complex IV (cytochrome c oxidase) activity. Conclusion In this pilot study, measurement can be performed in an appropriate timeline for clinical care with potential to serve as a prognostic marker. Further work is necessary to develop high-resolution respirometry as a clinical tool for assessing severity of illness and guiding therapy.

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“…More specifically, many researchers identified mitochondrial dysfunction as the key pathological change in septic cardiomyopathy. 21 , 22 Since the heart is one of the organs that is highly dependent on abundant adenosine triphosphate (ATP) levels to maintain its contraction and diastolic function, impaired mitochondrial function is lethally detrimental to the heart. According to cardiac pathophysiology, energy depletion resulting from mitochondrial dysfunction would contribute to significant myocardial damage, 23 such as diabetic cardiomyopathy, ischaemic reperfusion injury and heart failure.…”

Section: Introductionmentioning

confidence: 99%

The potential mechanism of mitochondrial dysfunction in septic cardiomyopathy

2018

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Septic cardiomyopathy is one of the most serious complications of sepsis or septic shock. Basic and clinical research has studied the mechanism of cardiac dysfunction for more than five decades. It has become clear that myocardial depression is not related to hypoperfusion. As the heart is highly dependent on abundant adenosine triphosphate (ATP) levels to maintain its contraction and diastolic function, impaired mitochondrial function is lethally detrimental to the heart. Research has shown that mitochondria play an important role in organ damage during sepsis. The mitochondria-related mechanisms in septic cardiomyopathy have been discussed in terms of restoring mitochondrial function. Mitochondrial uncoupling proteins located in the mitochondrial inner membrane can promote proton leakage across the mitochondrial inner membrane. Recent studies have demonstrated that proton leakage is the essential regulator of mitochondrial membrane potential and the generation of reactive oxygen species (ROS) and ATP. Other mechanisms involved in septic cardiomyopathy include mitochondrial ROS production and oxidative stress, mitochondria Ca2+ handling, mitochondrial DNA in sepsis, mitochondrial fission and fusion, mitochondrial biogenesis, mitochondrial gene regulation and mitochondria autophagy. This review will provide an overview of recent insights into the factors contributing to septic cardiomyopathy.

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Measurement of Mitochondrial Respiration and Motility in Acute Care

Cited by 40 publications

References 45 publications

Changing Metabolism in Differentiating Cardiac Progenitor Cells—Can Stem Cells Become Metabolically Flexible Cardiomyocytes?

Changing Metabolism in Differentiating Cardiac Progenitor Cells—Can Stem Cells Become Metabolically Flexible Cardiomyocytes?

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

The potential mechanism of mitochondrial dysfunction in septic cardiomyopathy

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