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Platelets from Asthmatic Individuals Show Less Reliance on Glycolysis.

Xu W, Cardenes N, Corey C, Erzurum SC, Shiva S - PLoS ONE (2015)

Bottom Line: Further, several studies demonstrate altered mitochondrial function in asthmatic airways and suggest that these changes may be systemic.However, it is unknown whether systemic metabolic changes can be detected in circulating cells in asthmatic patients.The implications for this potential metabolic shift will be discussed in the context of increased oxidative stress and hypoxic adaptation of asthmatic patients.

View Article: PubMed Central - PubMed

Affiliation: Lerner Research Institute, Cleveland, Ohio, United States of America.

ABSTRACT
Asthma, a chronic inflammatory airway disease, is typified by high levels of TH2-cytokines and excessive generation of reactive nitrogen and oxygen species, which contribute to bronchial epithelial injury and airway remodeling. While immune function plays a major role in the pathogenesis of the disease, accumulating evidence suggests that altered cellular metabolism is a key determinant in the predisposition and disease progression of asthma. Further, several studies demonstrate altered mitochondrial function in asthmatic airways and suggest that these changes may be systemic. However, it is unknown whether systemic metabolic changes can be detected in circulating cells in asthmatic patients. Platelets are easily accessible blood cells that are known to propagate airway inflammation in asthma. Here we perform a bioenergetic screen of platelets from asthmatic and healthy individuals and demonstrate that asthmatic platelets show a decreased reliance on glycolytic processes and have increased tricarboxylic acid cycle activity. These data demonstrate a systemic alteration in asthma and are consistent with prior reports suggesting that oxidative phosphorylation is more efficient asthmatic individuals. The implications for this potential metabolic shift will be discussed in the context of increased oxidative stress and hypoxic adaptation of asthmatic patients. Further, these data suggest that platelets are potentially a good model for the monitoring of bioenergetic changes in asthma.

No MeSH data available.


Related in: MedlinePlus

Platelets show no change in mitochondrial number and morphology in asthma.(A-B) Representative electron micrograph of platelet from (A) healthy control and (B) asthma (scale bars: 1 μm). (C) Mitochondrial DNA copy number per platelet in platelets from healthy and asthmatic individuals. n = 7 per group.
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pone.0132007.g002: Platelets show no change in mitochondrial number and morphology in asthma.(A-B) Representative electron micrograph of platelet from (A) healthy control and (B) asthma (scale bars: 1 μm). (C) Mitochondrial DNA copy number per platelet in platelets from healthy and asthmatic individuals. n = 7 per group.

Mentions: Electron microscopy of platelets from healthy and asthmatic individuals showed no overt differences in mitochondrial number or morphology (Fig 2A and 2B). Quantification of the number of mitochondria in each platelet demonstrated that there was no difference between the two groups (2.85 ± 0.40 vs 2.59 ± 0.38; asthma vs control; n = 10 platelets each from n = 4 subjects in each group). This was confirmed by measurement of mitochondrial DNA content in 7 different subjects in each group, which showed no significant changes in mitochondrial DNA copy number between groups (Fig 2C).


Platelets from Asthmatic Individuals Show Less Reliance on Glycolysis.

Xu W, Cardenes N, Corey C, Erzurum SC, Shiva S - PLoS ONE (2015)

Platelets show no change in mitochondrial number and morphology in asthma.(A-B) Representative electron micrograph of platelet from (A) healthy control and (B) asthma (scale bars: 1 μm). (C) Mitochondrial DNA copy number per platelet in platelets from healthy and asthmatic individuals. n = 7 per group.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4492492&req=5

pone.0132007.g002: Platelets show no change in mitochondrial number and morphology in asthma.(A-B) Representative electron micrograph of platelet from (A) healthy control and (B) asthma (scale bars: 1 μm). (C) Mitochondrial DNA copy number per platelet in platelets from healthy and asthmatic individuals. n = 7 per group.
Mentions: Electron microscopy of platelets from healthy and asthmatic individuals showed no overt differences in mitochondrial number or morphology (Fig 2A and 2B). Quantification of the number of mitochondria in each platelet demonstrated that there was no difference between the two groups (2.85 ± 0.40 vs 2.59 ± 0.38; asthma vs control; n = 10 platelets each from n = 4 subjects in each group). This was confirmed by measurement of mitochondrial DNA content in 7 different subjects in each group, which showed no significant changes in mitochondrial DNA copy number between groups (Fig 2C).

Bottom Line: Further, several studies demonstrate altered mitochondrial function in asthmatic airways and suggest that these changes may be systemic.However, it is unknown whether systemic metabolic changes can be detected in circulating cells in asthmatic patients.The implications for this potential metabolic shift will be discussed in the context of increased oxidative stress and hypoxic adaptation of asthmatic patients.

View Article: PubMed Central - PubMed

Affiliation: Lerner Research Institute, Cleveland, Ohio, United States of America.

ABSTRACT
Asthma, a chronic inflammatory airway disease, is typified by high levels of TH2-cytokines and excessive generation of reactive nitrogen and oxygen species, which contribute to bronchial epithelial injury and airway remodeling. While immune function plays a major role in the pathogenesis of the disease, accumulating evidence suggests that altered cellular metabolism is a key determinant in the predisposition and disease progression of asthma. Further, several studies demonstrate altered mitochondrial function in asthmatic airways and suggest that these changes may be systemic. However, it is unknown whether systemic metabolic changes can be detected in circulating cells in asthmatic patients. Platelets are easily accessible blood cells that are known to propagate airway inflammation in asthma. Here we perform a bioenergetic screen of platelets from asthmatic and healthy individuals and demonstrate that asthmatic platelets show a decreased reliance on glycolytic processes and have increased tricarboxylic acid cycle activity. These data demonstrate a systemic alteration in asthma and are consistent with prior reports suggesting that oxidative phosphorylation is more efficient asthmatic individuals. The implications for this potential metabolic shift will be discussed in the context of increased oxidative stress and hypoxic adaptation of asthmatic patients. Further, these data suggest that platelets are potentially a good model for the monitoring of bioenergetic changes in asthma.

No MeSH data available.


Related in: MedlinePlus