Inflammatory and oxidative stress phenotypes in transgenic sickle cell mice

Charrin, Emmanuelle; Ofori-Acquah, Solomon F.; Nader, Élie; Skinner, Sarah; Connes, Philippe; Pialoux, Vincent; Joly, Philippe; Martin, Cyril

doi:10.1016/j.bcmd.2016.10.020

Cited by 22 publications

(18 citation statements)

References 74 publications

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“…For example, AS mice demonstrated a mild increase in reticulocyte count and mild increase in LDH that may be due to a subclinical increase in haemolytic rate with reduced RBC lifespan. However, the levels of LDH and reticulocytes in both the AS and AA mice were still within the range of normal values expected for these mouse strains and in agreement with other recent data (Charrin et al , ). Though Charrin et al () observed no differences between Townes AA and AS reticulocyte counts, they utilized a different method (manual counting after brilliant cresyl blue staining) and reported levels much lower than had been previously reported (Wu et al , ), both of which may contribute to the differences in our results compared to those reported by Charrin et al ().…”

Section: Discussionsupporting

confidence: 92%

Characterization of a mouse model of sickle cell trait: parallels to human trait and a novel finding of cutaneous sensitization

et al. 2017

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Sickle cell trait (SCT) has classically been categorized as a benign condition except in rare cases or upon exposure to severe physical conditions. However, several lines of evidence indicate that individuals with SCT are not always asymptomatic, and additional physiological changes and risks may remain unexplored. Here, we utilized mice harbouring one copy of normal human β globin and one copy of sickle human β globin as a model of SCT, to assess haematological, histopathological and somatosensory outcomes. We observed that SCT mice displayed renal and hepatic vascular congestion after exposure to hypoxia. Further, we observed that SCT mice displayed increased cold aversion as well as mechanical and heat sensitivity, though to a lesser degree than homozygous sickle cell disease mice. Notably, mechanical hypersensitivity increased following hypoxia and reoxygenation. Overall our findings suggest that SCT is not entirely benign, and further assessment of pain and cutaneous sensitization is warranted both in animal models and in clinical populations.

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Section: Discussionsupporting

confidence: 92%

Characterization of a mouse model of sickle cell trait: parallels to human trait and a novel finding of cutaneous sensitization

et al. 2017

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“…The tibialis anterior muscle of all the mice was homogenized (10 %, w/v) in 1× PBS plus 0.5 m m EDTA in ice. After centrifugation (10 min, 12,000 g , 4°C), the supernatant was collected for measurement of oxidative stress and antioxidant markers, as previously described (Charrin et al., ). Homogenate aliquots were stored at −80°C.…”

Section: Methodsmentioning

confidence: 99%

“…oxidative stress and antioxidant markers, as previously described (Charrin et al, 2016). Homogenate aliquots were stored at −80 • C.…”

Section: Oxidative Stress and Antioxidant Assessmentmentioning

confidence: 99%

Ischaemia‐induced muscle metabolic abnormalities are poorly alleviated by endurance training in a mouse model of sickle cell disease

Chatel

Messonnier

Vilmen

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?The aim of this study was to evaluate the potential beneficial effects of endurance training during an ischaemia–reperfusion protocol in a mouse model of sickle cell disease (SCD). What is the main finding and its importance?Endurance training did not reverse the metabolic defects induced by a simulated vaso‐occlusive crisis in SCD mice, with regard to intramuscular acidosis, mitochondrial dysfunction or anatomical properties. Our results suggest that endurance training would reduce the number of vaso‐occlusive crises rather than the complications related to vaso‐occlusive crises. Abstract The aim of this study was to investigate whether endurance training could limit the abnormalities described in a mouse model of sickle cell disease (SCD) in response to an ischaemia–reperfusion (I/R) protocol. Ten sedentary (HbSS‐SED) and nine endurance‐trained (HbSS‐END) SCD mice were submitted to a standardized protocol of I/R of the leg, during which ATP, phosphocreatine and inorganic phosphate concentrations and intramuscular pH were measured using magnetic resonance spectroscopy. Forty‐eight hours later, skeletal muscles were harvested. Oxidative stress markers were then measured. Although the time course of protons accumulation was slightly different between trained and sedentary mice (P < 0.05), the extent of acidosis was similar at the end of the ischaemic period. The initial rate of phosphocreatine resynthesis measured at blood flow restoration, illustrating mitochondrial function, was not altered in trained mice compared with sedentary mice. Although several oxidative stress markers were not different between groups (P > 0.05), the I/R‐related increase of uric acid concentration observed in sedentary SCD mice (P < 0.05) was not present in the trained group. The spleen weight, generally used as a marker of the severity of the disease, was not different between groups (P > 0.05). In conclusion, endurance training did not limit the metabolic consequences of an I/R protocol in skeletal muscle of SCD mice, suggesting that the reduction in the severity of the disease previously demonstrated in the basal state would be attributable to a reduction of the occurrence of vaso‐occlusive crises rather than a decrease of the deleterious effects of vaso‐occlusive crises.

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“…Recent studies have reported a number of biological abnormalities in SCT mice, including kidney damage and increased oxidative stress. 4,5 Considering the alterations in vascular health and macrovascular function that have been observed in individuals with SCT, it seems pertinent to determine whether macrovascular reactivity is also altered in SCT mice. Therefore, this study evaluated vascular reactivity in the aortae, mesenteric arteries and femoral arteries of a mouse model of SCT.…”

Section: Alterations In Vascular Reactivity In a Transgenic Mouse Modmentioning

confidence: 99%

Alterations in vascular reactivity in a transgenic mouse model of sickle cell trait

et al. 2020

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Inflammatory and oxidative stress phenotypes in transgenic sickle cell mice

Cited by 22 publications

References 74 publications

Characterization of a mouse model of sickle cell trait: parallels to human trait and a novel finding of cutaneous sensitization

Characterization of a mouse model of sickle cell trait: parallels to human trait and a novel finding of cutaneous sensitization

Ischaemia‐induced muscle metabolic abnormalities are poorly alleviated by endurance training in a mouse model of sickle cell disease

Alterations in vascular reactivity in a transgenic mouse model of sickle cell trait

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