Sickle cell disease (SCD) is characterized by painful vaso-occlusive crisis. While there are several metabolic abnormalities potentially associated with muscular ischemia–reperfusion cycles that could be harmful in the context of SCD, the metabolic consequences of such events are still unknown. Ten controls (HbAA), thirteen heterozygous (HbAS), and ten homozygous (HbSS) SCD mice were submitted to a standardized protocol of rest–ischemia–reperfusion of the left leg during which adenosine triphosphate, phosphocreatine, and inorganic phosphate concentrations as well as intramuscular pH were measured using phosphorous magnetic resonance spectroscopy (MRS). Forty-eight hours later, skeletal muscles were harvested. Oxidative stress markers were then measured on the tibialis anterior. At the end of the ischemic period, HbSS mice had a lower pH value as compared with the HbAA and HbAS groups (P<0.01). During the reperfusion period, the initial rate of phosphocreatine resynthesis was lower in HbSS mice as compared with HbAA (P<0.05) and HbAS (P<0.01) animals. No significant difference among groups was observed regarding oxidative stress markers. HbSS mice displayed a higher intramuscular acidosis during the ischemic period while their mitochondrial function was impaired as compared with their HbAA and HbAS counterparts. These metabolic abnormalities could worsen the complications related to the pathology of SCD.
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October 2018
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In this issue, Wohlfahrtova et al. report on the link between early isolated v-lesion (eIV) and rejection of kidney allografts. The cover image is a Circos plot that depicts the association between the 15 most signifi cant up-regulated genes between TCMRV (T cell-mediated vascular rejection) and eIV, and signifi cantly enriched pathways and GO terms that play a role in the immune response. For further details, see pages 2269–2284 .
Research Article|
October 02 2018
Exacerbated metabolic changes in skeletal muscle of sickle cell mice submitted to an acute ischemia–reperfusion paradigm
Benjamin Chatel;
1Aix-Marseille Univ, CNRS, CRMBM, Marseille, France
2Univ Savoie Mont Blanc, Laboratoire Interuniversitaire de Biologie de la Motricité, EA 7424, F-73000 Chambéry, France
Correspondence: Benjamin Chatel ([email protected])
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Laurent A. Messonnier;
Laurent A. Messonnier
2Univ Savoie Mont Blanc, Laboratoire Interuniversitaire de Biologie de la Motricité, EA 7424, F-73000 Chambéry, France
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Christophe Vilmen;
Christophe Vilmen
1Aix-Marseille Univ, CNRS, CRMBM, Marseille, France
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Monique Bernard;
Monique Bernard
1Aix-Marseille Univ, CNRS, CRMBM, Marseille, France
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Vincent Pialoux;
Vincent Pialoux
3Univ Lyon, UCBL1, Laboratoire Interuniversitaire de Biologie de la Motricité, EA 7424, Villeurbanne, France
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David Bendahan
David Bendahan
1Aix-Marseille Univ, CNRS, CRMBM, Marseille, France
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Publisher: Portland Press Ltd
Received:
March 28 2018
Revision Received:
August 27 2018
Accepted:
September 05 2018
Accepted Manuscript online:
September 05 2018
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2018
Clin Sci (Lond) (2018) 132 (19): 2103–2115.
Article history
Received:
March 28 2018
Revision Received:
August 27 2018
Accepted:
September 05 2018
Accepted Manuscript online:
September 05 2018
Citation
Benjamin Chatel, Laurent A. Messonnier, Christophe Vilmen, Monique Bernard, Vincent Pialoux, David Bendahan; Exacerbated metabolic changes in skeletal muscle of sickle cell mice submitted to an acute ischemia–reperfusion paradigm. Clin Sci (Lond) 15 October 2018; 132 (19): 2103–2115. doi: https://doi.org/10.1042/CS20180268
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