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See detailA water-soluble salt of curcumin (NDS27) inhibits myeloperoxidase and NADPH oxidase activities, two major enzymes of neutrophils.
Derochette, Sandrine ULiege; Mouithys-Mickalad, Ange ULiege; Deby-Dupont, Ginette et al

Poster (2013, September 11)

Neutrophils (PMNs) produce reactive oxygen species (ROS) to kill pathogenic agents. After appropriate stimulation, leading to the activation of protein kinase C (PKC), the cytosolic subunits of the NADPH ... [more ▼]

Neutrophils (PMNs) produce reactive oxygen species (ROS) to kill pathogenic agents. After appropriate stimulation, leading to the activation of protein kinase C (PKC), the cytosolic subunits of the NADPH oxidase (Nox2) are phosphorylated and translocated to the membrane flavocytochrome b558, forming the active enzyme which produces superoxide anion (O2●-). From O2●- derives H2O2 used by the PMNs myeloperoxidase (MPO) to form strong oxidant species. Many human and animal pathologies with fatal issue are associated with uncontrolled activation of PMNs. The modulation of enzymes implied in ROS production is thus a primary target to manage excessive inflammatory events. For this purpose, we evaluated the effects of NDS27, a water-soluble salt of curcumin combined with hydroxypropyl-β-cyclodextrin, on the activities of PKC, Nox2 and MPO. PKC activation was determined by western blotting with specific antibodies against phosphorylated PKC in extracts from PMNs after their incubation or not with NDS27. A cell-free assay was used to evaluate the effect of NDS27 before or after the assembly of Nox2 subunits. MPO activity was tested by the SIEFED technique in which NDS27 was pre-incubated with the enzyme and discarded before its activity measurement. An inhibition of PKC phosphorylation and Nox2 activity were observed at respectively 10-4 and 10-5 M of NDS27. The Nox2 inhibition was more pronounced when NDS27 was added before the assembly stimulation, suggesting a direct action of NDS27 on the subunits translocation. NDS27 also dose-dependently decreased the activity of MPO (21 % at 10-5 M), indicating an interaction with the enzyme structure. Our results demonstrated that NDS27 is a potent inhibitor of the two major enzymes responsible for ROS production in PMNs, and also acts on the activation cascade of Nox2. The modulatory effect of NDS27 towards the oxidant activity of PMNs opens therapeutic perspectives to control pathologies with excessive inflammatory reactions. [less ▲]

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See detailNew 5-Aryl-1H-imidazoles display in vitro antitumor activity against apoptosis-resistant cancer models, including melanomas, through mitochondrial targeting.
Mathieu, Véronique; Van Den Brege, E; Ceusters, Justine ULiege et al

in Journal of Medicinal Chemistry (2013), 56(17), 6626-6637

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See detailThe challenge of understanding myopathies in horses using permeabilized muscle cells
Votion, Dominique ULiege; Mouithys-Mickalad, Ange ULiege; Ceusters, Justine ULiege et al

in In proceedings 9th Conference on Mitochondrial Physiology (2013, September)

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See detailSensitivity and specificity of blood leukocyte counts as an indicator of mortality in horses after colic surgery
Salciccia, Alexandra ULiege; Sandersen, Charlotte ULiege; Grulke, Sigrid ULiege et al

in Veterinary Record : Journal of the British Veterinary Association (2013), 173(11),

The objectives of this study were to describe and relate perioperative changes in blood leukocyte counts to the outcome of surgical colic horses, determine a cut-off value in the early postoperative ... [more ▼]

The objectives of this study were to describe and relate perioperative changes in blood leukocyte counts to the outcome of surgical colic horses, determine a cut-off value in the early postoperative period to obtain an indicator of the outcome, and compare the obtained value to a validation population of horses. Fifty-three horses undergoing colic surgery were included in the descriptive part of the study. Total leukocyte counts were performed before, during and serially after surgery. A receiver operating characteristic analysis was performed on the leukocyte counts of 45 of these horses to determine a cut-off value for the outcome. The results obtained were validated on a second set of 50 horses that underwent colic surgery in similar conditions. The kinetics of blood leukocytes in survivors was higher than in non-survivors during the first days. Non-survivor horses were more likely to have at least one blood leukocyte count ≤3.9×103/mm3 between 28 and 60 hours after surgery than survivor horses. This cut-off value was confirmed in the validation population. These results suggest that routine values of blood leukocyte counts can be used as an additional prognostic indicator after colic surgery alongside other predictors previously associated with the outcome. [less ▲]

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See detailPrédiction des performances sportives et détection précoce des myopathies par respirométrie à haute résolution
Votion, Dominique ULiege; Serteyn, Didier ULiege

in cheval athlète, stress oxydant & inflammation (2013, June 07)

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See detailIdentification of methylenecyclopropyl acetic acid in serum of European horses with atypical myopathy
Votion, Dominique ULiege; van Galen, G; Sweetan et al

in Equine Veterinary Journal (2013)

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See detailMitochondrial dysfunction in HDAC5-depleted cancer cells induces glucose-dependent metabolic adaptation
Hendrick, Elodie ULiege; Matheus, Nicolas ULiege; Peixoto, Paul ULiege et al

Poster (2013, May 17)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes, which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad-spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis1. Aims: The goal of this study is to further investigate the molecular mechanisms by which HDAC5 depletion induces both autophagy and apoptosis in cancer cells. Results: Screening transcriptomic study demonstrated that HDAC5 depletion induces a deregulation of genes encoding subunits of complex I of the mitochondrial respiratory chain leading to a significant increase of ROS production. This ROS accumulation promotes autophagy including mitophagy. Indeed, pretreatment with NAC, a ROS scavenger, blocked autophagy triggered by HDAC5 silencing. This autophagy seems to be protective as its blocking with NAC, chloroquine or bafilomycin A1 enhances pro-apoptotic effect of HDAC5 depletion. In addition, mitochondrial dysfunction provokes metabolism adaptation associated with increase of the importance of glucose metabolism in HDAC5 depleted cancer cells. Indeed, low-glucose culture of HDAC5-depleted cells significantly increases apoptotic cell death suggesting that glucose deprivation might be combined to HDAC5 inhibition as a therapeutic strategy to kill cancer cells. Conclusion: Our study demonstrated for the first time that specific HDAC5 inhibition induces alteration of gene expression encoding mitochondrial proteins in cancer cells and provide insight into a valuable experimental strategy for manipulation of specific HDAC5 inhibition and glucose metabolism in therapy against cancer. 1.Peixoto, P. et al. HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells. Cell death and differentiation, 2012; 1-14. [less ▲]

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See detailMyeloperoxidase activity decreases in equine semen freezing extenders
Ponthier, Jérôme ULiege; Franck, Thierry ULiege; Niesten, Ariane ULiege et al

in Amir, Arav (Ed.) Proceedings of the 3rd Cryo Congress (2013, March 23)

Myeloperoxidase (MPO) is a pro-oxidant enzyme contained in and released by neutrophils, and associated with decreased post-thaw motility of equine semen. This study aimed to compare MPO activity in pure ... [more ▼]

Myeloperoxidase (MPO) is a pro-oxidant enzyme contained in and released by neutrophils, and associated with decreased post-thaw motility of equine semen. This study aimed to compare MPO activity in pure equine freezing extender, raw and post-thaw semen. Active MPO Concentration (AMC) was measured with Specific Immunologic Extraction Followed by Enzymatic Detection in 20 ejaculates. Raw semen intra cellular AMC was determined in the supernatant after membrane lysis, each pellet containing 100x106 spermatozoa. AMC was also assayed in supernatants of semen frozen following a conventional method using INRA FreezeTM (IMV, France). Effect of freezing procedure on AMC was tested by experimentally adding 500ng of purified active MPO (Calbiochem, Germany) in 4 samples either with 5ml of PBS or INRA FreezeTM before assay. AMC was higher in sperm-rich pellet (0.306ng/ml) than in post-thaw semen (0.002ng/ml) (p=0.058). After experimental MPO addition, no activity variation was observed during the freezing procedure (after dilution, 1, 2 hours of cooling and post-thawing) within the same medium. Purified MPO activity was decreased in INRA FreezeTM when compared to PBS at all timings of sampling (p=0.0286). When all samples were pooled, remaining activity in INRA FreezeTM was 23.93±13.13%. MPO fixation on large proteins contained in the extender experimentally reduces AMC, as previously observed in plasma. However, AMC decrease observed during semen freezing is more important than after experimental addition. That could be explained by a MPO interaction with seminal plasma, a partial MPO release or a MPO inactivation during equine semen freezing. [less ▲]

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See detailJNK/ROS signaling pathway is responsible for induction of autophagy in HDAC5 depleted cancer cells
Hendrick, Elodie ULiege; Mathéus, Nicolas; Peixoto, Paul ULiege et al

Poster (2013, February 02)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis (ref papier). The study of autophagy in cancer is a new research field that has recently generated tremendous attention due to the recognition that autophagy can have either pro-survival or pro-death functions depending on its level of activation. In addition, more and more studies indicate that a complex relationship exists between autophagy and apoptosis, and that the interplay between these two processes determines whether a cell will live or die. Aims: The goal of this study is to further understand the role of autophagy induced by HDAC5 depletion. Current investigations include determining the molecular mechanisms by which HDAC5 depletion induces autophagy and exploring regulatory relationship between autophagy and apoptosis on cancer cell death in absence of HDAC5. Results: The set up of the autophagy in absence of HDAC5 was demonstrated by the conversion of LC3 and development of autophagosomes by electronic microscopy. Transcriptomic study demonstrated a deregulation of a set of genes involved in ROS detoxification in HDAC5 depleted cancer cells leading to significant increase of ROS levels. Further investigations showed that pretreatment with NAC, a ROS scavenger, effectively blocked the accumulation of ROS and autopahgy triggered by HDAC5 silencing. Moreover, HDAC5 depletion induces activation of JNK, and knockdown of JNK by siRNA inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by HDAC5 depletion indicating that JNK activation may be a upstream signaling of ROS and should be a core component in HDAC5 silencing-induced autophagic signaling pathway. Finally, blocking of autophagy induced by HDAC5 silencing with NAC or chloroquine and bafilomycin enhanced pro-apoptotic effect. Conclusion: Autophagy functions as a prosurvival mechanism to mitigate HDAC5 depletion-induced apoptotic cell death, suggesting that targeting autophagy might improve the therapeutic effects of specific HDAC5 inhibition. [less ▲]

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See detailJNK/ROS Signaling Pathway Is Responsible for Induction of Autophagy in HDAC5 depleted Cancer Cells
Hendrick, Elodie ULiege; Mathéus, Nicolas; Peixoto, Paul ULiege et al

Conference (2013, January 29)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis (ref papier). The study of autophagy in cancer is a new research field that has recently generated tremendous attention due to the recognition that autophagy can have either pro-survival or pro-death functions depending on its level of activation. In addition, more and more studies indicate that a complex relationship exists between autophagy and apoptosis, and that the interplay between these two processes determines whether a cell will live or die. Aims: The goal of this study is to further understand the role of autophagy induced by HDAC5 depletion. Current investigations include determining the molecular mechanisms by which HDAC5 depletion induces autophagy and exploring regulatory relationship between autophagy and apoptosis on cancer cell death in absence of HDAC5. Results: The set up of the autophagy in absence of HDAC5 was demonstrated by the conversion of LC3 and development of autophagosomes by electronic microscopy. Transcriptomic study demonstrated a deregulation of a set of genes involved in ROS detoxification in HDAC5 depleted cancer cells leading to significant increase of ROS levels. Further investigations showed that pretreatment with NAC, a ROS scavenger, effectively blocked the accumulation of ROS and autopahgy triggered by HDAC5 silencing. Moreover, HDAC5 depletion induces activation of JNK, and knockdown of JNK by siRNA inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by HDAC5 depletion indicating that JNK activation may be a upstream signaling of ROS and should be a core component in HDAC5 silencing-induced autophagic signaling pathway. Finally, blocking of autophagy induced by HDAC5 silencing with NAC or chloroquine and bafilomycin enhanced pro-apoptotic effect. Conclusion: Autophagy functions as a prosurvival mechanism to mitigate HDAC5 depletion-induced apoptotic cell death, suggesting that targeting autophagy might improve the therapeutic effects of specific HDAC5 inhibition. [less ▲]

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See detailJNK/ROS signaling pathway is responsible for induction of autophagy in HDAC5 depleted cancer cells
Hendrick, Elodie ULiege; Mathéus, Nicolas; Peixoto, Paul ULiege et al

Poster (2013, January 28)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis (ref papier). The study of autophagy in cancer is a new research field that has recently generated tremendous attention due to the recognition that autophagy can have either pro-survival or pro-death functions depending on its level of activation. In addition, more and more studies indicate that a complex relationship exists between autophagy and apoptosis, and that the interplay between these two processes determines whether a cell will live or die. Aims: The goal of this study is to further understand the role of autophagy induced by HDAC5 depletion. Current investigations include determining the molecular mechanisms by which HDAC5 depletion induces autophagy and exploring regulatory relationship between autophagy and apoptosis on cancer cell death in absence of HDAC5. Results: The set up of the autophagy in absence of HDAC5 was demonstrated by the conversion of LC3 and development of autophagosomes by electronic microscopy. Transcriptomic study demonstrated a deregulation of a set of genes involved in ROS detoxification in HDAC5 depleted cancer cells leading to significant increase of ROS levels. Further investigations showed that pretreatment with NAC, a ROS scavenger, effectively blocked the accumulation of ROS and autopahgy triggered by HDAC5 silencing. Moreover, HDAC5 depletion induces activation of JNK, and knockdown of JNK by siRNA inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by HDAC5 depletion indicating that JNK activation may be a upstream signaling of ROS and should be a core component in HDAC5 silencing-induced autophagic signaling pathway. Finally, blocking of autophagy induced by HDAC5 silencing with NAC or chloroquine and bafilomycin enhanced pro-apoptotic effect. Conclusion: Autophagy functions as a prosurvival mechanism to mitigate HDAC5 depletion-induced apoptotic cell death, suggesting that targeting autophagy might improve the therapeutic effects of specific HDAC5 inhibition. [less ▲]

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See detailIntra- and extracellular antioxidant capacities of the new water-soluble form of curcumin (NDS27) on stimulated neutrophils and HL-60 cells
Derochette, Sandrine ULiege; Franck, Thierry ULiege; Mouithys-Mickalad, Ange ULiege et al

in Chemico-Biological Interactions (2013), 201(1-3), 49-57

Phagocytic cells, especially neutrophils (PMNs) are specialized in the production of reactive oxygen species (ROS) to kill pathogenic agents, but an excessive ROS production is associated with tissue ... [more ▼]

Phagocytic cells, especially neutrophils (PMNs) are specialized in the production of reactive oxygen species (ROS) to kill pathogenic agents, but an excessive ROS production is associated with tissue damages and inflammatory diseases. Phagocytes are thus prime therapeutic targets to control inflammatory events associated to ROS production. Nowadays, there is a growing interest for the use of polyphenols to modulate the inflammatory response. The aim of this work was to study the antioxidant effect of NDS27, a highly water-soluble form of the polyphenolic molecule curcumin, on in vitro stimulated equine PMNs and human promyelocytic leukemia cells (HL-60). NDS27 was either pre-incubated with cells and eliminated before their activation (intracellular effect) or let in the medium (extracellular effect). Our results indicate that NDS27 significantly and dose-dependently (10 6 M–10 4 M) inhibited the ROS production in both cell types without affecting their viability. NDS27 was able to cross and interact with cell membrane, especially for HL-60 cells, while we observed a better intracellular antioxidant effect with PMNs. The activity of myeloperoxidase (MPO) released by PMNs and HL-60 cells, was decreased by NDS27, but more efficiently for PMNs. These results suggested that the greater efficiency of NDS27 in PMNs is due to an inhibitory effect on cells which are more mature for ROS production, probably by targeting the enzymes implied in respiratory burst like MPO. The modulatory effect of NDS27 on the oxidant activity of cells involved in immune and inflammatory responses opens perspectives for a therapeutic control of pathologies with excessive inflammatory reactions. [less ▲]

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See detailEquine myeloperoxidase: A novel biomarker in synovial fluid for the diagnosis of infection.
Wauters, J.; Pille, F.; Martens, A. et al

in Equine Veterinary Journal (2013), 45(3),

REASONS FOR PERFORMING STUDY: Equine joint infection is a life-threatening disorder, and confirmation of the diagnosis can be difficult. Synovial fluid biomarkers may assist the discrimination between ... [more ▼]

REASONS FOR PERFORMING STUDY: Equine joint infection is a life-threatening disorder, and confirmation of the diagnosis can be difficult. Synovial fluid biomarkers may assist the discrimination between infectious and noninfectious joint disease. OBJECTIVES: This study investigates whether the immunological detection of total and enzymatically active myeloperoxidase (MPO) assists the diagnosis of joint infection in horses. METHODS: The following 4 sample groups were included: healthy; osteochondritis dissecans (OCD); traumatic synovitis; and culture-confirmed infected joints. Synovial fluid was analysed for total MPO by a horse-specific sandwich enzyme-linked immunosorbent assay (ELISA) and for active MPO using the specific immunological extraction followed by enzymatic detection (SIEFED) technique. Western blot analysis was performed to confirm the antibody specificity. RESULTS: Synovial fluid from infected joints contained significantly more total and active MPO than samples from healthy joints, joints affected by OCD and joints with traumatic synovitis. Cut-off values were set at 5000 and 350 ng/ml for total and active MPO, respectively, with fair sensitivity, specificity, positive and negative predictive values and likelihood ratios for infection. Correlation coefficients were reported between the total as well as the active MPO levels and the routine synovial fluid parameters, i.e. the white blood cell count, the neutrophil count and the total protein level. No correlation was observed between MPO and either the age of the horse or the joint affected. Western blotting confirmed the antibody specificity for equine MPO. CONCLUSIONS AND POTENTIAL RELEVANCE: Synovial fluid MPO was identified as a very promising biomarker to augment the discrimination of infectious vs. noninfectious joint disease in horses. Both ELISA and SIEFED techniques can be used for its specific and rapid detection. The analysis of synovial fluid MPO can be used as a complementary test to aid in the discrimination between infectious and noninfectious joint disease, especially when the white blood cell counts and the total protein level are inconclusive. [less ▲]

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See detailSystemic Active and Total Myeloperoxidase Levels in Coronary Artery Disease.
GACH, Olivier ULiege; MAGNE, Julien ULiege; Franck, Thierry ULiege et al

in Cardiology (2013), 126(Suppl. 2), 1-521

Backgound: Measurement of total Myeloperoxidase (MPO) by ELISA is considered as a marker of neutrophil activation but is not the true indicator of the degree of its activity. In a dynamic pathology such ... [more ▼]

Backgound: Measurement of total Myeloperoxidase (MPO) by ELISA is considered as a marker of neutrophil activation but is not the true indicator of the degree of its activity. In a dynamic pathology such as atherosclerosis, it may be important to measure the real active part of MPO because it represents the true witness of the oxidant potential of the enzyme. Aim: To identify the relation between coronary artery disease identified by coronaro-angiography on measured serum total and active MPO levels and evaluate the correlation between these MPO levels and the presence of clinically defined unstable condition. Methods: Prospective analyse of serum samples of patients before (within 30 min) coronaro-angiography. Total and active MPO concentrations were assessed by sandwich Elisa and SIEFED® method’s respectively. Results: Two hundred and twenty patients were included in this study (age: 66.1±10.7 years, 67% of male). Among these, 62% presented significant coronary artery disease (stenosis more than 60% at least in one épicardial coronary artery). Twenty four patients (11%) presented unstable coronary syndrome. Mean active and total MPO in the general population were 50.1±63.5 and 147.6±223.3 ng.mL-1 respectively. In comparison, mean active MPO was 47.1±47.9 ng.mL-1 in stable patients and 75.1±135.2 ng.mL-1 in unstable patients (p=0.04). Mean total MPO was 146.3±224.7 ng.mL-1 in stable patients and 158.2±215.8 ng.mL-1 in the unstable’s one (p=0.8). There was a significant correlation between active MPO levels and instability (r=0.14, p=0.04) not present for total MPO levels (r=0.016, p=0.8). Conclusion: We observed a correlation between active MPO and clinical instability while there was no correlation with total MPO. Our preliminary results suggest that this marker could be a powerful indicator of instability which could possess an important prognostic impact. This hypothesis requires an evaluation in wider population and during a prolonged follow-up. [less ▲]

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See detailDo developmental orthopaedic disorders influence future jumping performances in Warmblood stallions?
Verwilghen, D. R.; Janssens, S.; Busoni, Valeria ULiege et al

in Equine veterinary journal (2013), 45(5), 578-81

REASONS FOR PERFORMING THE STUDY: Few reports are available on the relationship between developmental orthopaedic diseases (DOD) and future performances in Warmblood horses. OBJECTIVES: To investigate the ... [more ▼]

REASONS FOR PERFORMING THE STUDY: Few reports are available on the relationship between developmental orthopaedic diseases (DOD) and future performances in Warmblood horses. OBJECTIVES: To investigate the relationship between performance and the presence of DOD lesions. METHODS: Records of Warmblood stallions for which radiographic and performance data were available were collected. Showjumping performances were expressed as scores derived from the final ranking of horses in each competition. These scores are available in an established performance database. The relationship between radiographic findings and both performance scores and number of performances was analysed using a linear regression model. RESULTS: Two hundred and fifteen horses met the inclusion criteria. There was no difference in either the number of performances or performance score between horses categorised as affected with DOD lesions (independent of joint location) compared with controls. Significantly lower numbers of performances were recorded for horses with osteochondral fragments (OCD) located at the dorsal aspect of the sagittal ridge of the metacarpo/metatarsophalangeal bone. No significant difference was found between horses affected with DOD lesions of the tarsocrural joint and controls. Horses with osteochondrosis of the lateral trochlear ridge of the femur had both significantly lower performance scores and numbers of performances compared with controls. CONCLUSION: This study demonstrated that specific DOD location and site within the joint have an influence on performance. Osteochondral fragments in the femoropatellar and at the dorsal aspect of the sagittal ridge of the metacarpo/metatarsophalangeal joint resulted in lowered performance. Fragmentation in the tarsocrural joint had no influence on performance. POTENTIAL RELEVANCE: The future athletic performance of Warmblood jumping horses may be limited as a result of OCD in the femoropatellar joint and to a certain extent the metacarpo/metatarsophalangeal joint. [less ▲]

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See detailEvaluation of acepromazine-induced hemodynamic alterations and reversal with norepinephrine infusion in standing horses
Pequito, Manuel; Amory, Hélène ULiege; De Moffarts, Brieux et al

in Canadian Veterinary Journal = Revue Vétérinaire Canadienne (2013), 54

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See detailOsteochondosis in foals
Sandersen, Charlotte ULiege; Vander Heyden, Laurent ULiege; Detilleux, Johann ULiege et al

in Veterinary Record : Journal of the British Veterinary Association (2013), 127(17), 456-467

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See detailCurcumin and resveratrol act by different ways on NADPH oxidase activity and reactive oxygen species produced by equine neutrophils
Derochette, Sandrine ULiege; Franck, Thierry ULiege; Mouithys-Mickalad, Ange ULiege et al

in Chemico-Biological Interactions (2013), 206

In neutrophils (PMNs), superoxide anion (O2●-), the first reactive oxygen species (ROS) produced to kill pathogenic agents, is generated by NADPH oxidase, an enzymatic complex formed by the translocation ... [more ▼]

In neutrophils (PMNs), superoxide anion (O2●-), the first reactive oxygen species (ROS) produced to kill pathogenic agents, is generated by NADPH oxidase, an enzymatic complex formed by the translocation of cytosolic subunits to the membrane flavocytochrome b558. In horses, excessive activation of PMNs is often associated with deadly pathologies and the modulation of their ROS production by acting on NADPH oxidase is a prime target to manage inflammation. We developed a cell-free assay to measure the activity of equine NADPH oxidase assembled in vitro, in order to test the effects of natural or synthetic compounds on the enzyme activity or assembly. The cell-free assay was validated with diphenyleneiodonium chloride and Gp91ds-tat, two inhibitors largely described for human NADPH oxidase. The anti-oxidant effects of curcumin and resveratrol at final concentration ranging from 10-4 to 10-6 M were studied on whole cells by chemiluminescence (CL) and by cell-free assay, in which the molecule was added before or after the enzyme assembly. The CL assay demonstrated that curcumin efficiently inhibited the O2●- production and easily entered into PMNs or interacted with their membrane. Cell-free assay showed that curcumin acted on the reconstitution of NADPH oxidase even at 10-5 M, while resveratrol appeared to be an O2●- scavenger rather than an inhibitor of NADPH oxidase activity, since it acted from outside the cell in CL and after the complex assembly in cell-free assay. By acting directly on NADPH oxidase, curcumin should be a good candidate for the treatment of acute or inflammatory diseases involving an excessive ROS production. [less ▲]

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See detailEffect of myeloperoxidase and anoxia/reoxygenation on mitochondrial respiratory function of cultured primary equine skeletal myoblasts.
Ceusters, Justine ULiege; Mouithys-Mickalad, Ange ULiege; Franck, Thierry ULiege et al

in Mitochondrion (2013), 13(5),

Horses are particularly sensitive to excessive inflammatory reaction where myeloperoxidase, a marker of inflammation, may contribute to mitochondrial dysfunctions. This study investigated the interaction ... [more ▼]

Horses are particularly sensitive to excessive inflammatory reaction where myeloperoxidase, a marker of inflammation, may contribute to mitochondrial dysfunctions. This study investigated the interaction between myeloperoxidase and cultured primary equine skeletal myoblasts, particularly its effect on mitochondrial respiration combined or not with anoxia followed by reoxygenation (AR). We showed that active myeloperoxidase entered into the cells, interacted with mitochondria and decreased routine and maximal respirations. When combined with AR, myeloperoxidase caused a further decrease of these respiratory parameters while the leak increased. Our results indicate that myeloperoxidase amplifies the mitochondrial damages initiated by AR phenomenon and alters the mitochondrial function. [less ▲]

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See detailAssociation of breeding conditions with prevalence of osteochondrosis in foals
Vander Heyden, Laurent ULiege; Lejeune, Jean-Philippe ULiege; Caudron, Isabelle ULiege et al

in Veterinary Record : Journal of the British Veterinary Association (2013), 178

Osteochondrosis (OC) is the most common developmental orthopaedic disease in horses and represents a major problem to the horse industry. The complete mechanism of this multifactorial disease is not yet ... [more ▼]

Osteochondrosis (OC) is the most common developmental orthopaedic disease in horses and represents a major problem to the horse industry. The complete mechanism of this multifactorial disease is not yet elucidated, but it is accepted that OC lesions are the result of intrinsic genetic and external factors. The aim of the present work was to evaluate the relationship between breeding management and OC. Breeding conditions were recorded, and a radiological examination was performed in 223 foals. Feeding practice and housing management were analysed in a multivariate model to determine risk factors for OC in three periods: gestation, birth to weaning and weaning to one-year-old. The major breakthrough of this study is the significant relationship between OC development and (1) the maternal nutrition during gestation and (2) the type of housing of the foals during their first year. It appears that mares fed with concentrates during gestation are more likely to produce foals that are subsequently affected by OC compared with other mares (P<0.05). Foals housed exclusively at pasture until one year of age are significantly less affected than foals exclusively housed in box or, alternatively, in box and at pasture (P<0.05). These results underline the role of the energy metabolism and the level of exercise in the aetiologic process of the disease, and help to develop preventive strategies during the crucial period of gestation to one year of age of the foal. [less ▲]

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