Laboratory of Medical Biochemistry

science, Belgium

Laboratory of Medical Biochemistry

science, Belgium
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Vliegen G.,Laboratory of Medical Biochemistry | Raju T.K.,Laboratory of Medical Biochemistry | Adriaensen D.,University of Antwerp | Lambeir A.-M.,Laboratory of Medical Biochemistry | de Meester I.,Laboratory of Medical Biochemistry
Annals of Translational Medicine | Year: 2017

The pathophysiology of lung diseases is very complex and proteolytic enzymes may play a role or could be used as biomarkers. In this review, the literature was searched to make an overview of what is known on the expression of the proline-specific peptidases dipeptidyl peptidase (DPP) 4, 8, 9, prolyl oligopeptidase (PREP) and fibroblast activation protein A (FAP) in the healthy and diseased lung. Search terms included asthma, chronic obstructive pulmonary disease (COPD), lung cancer, fibrosis, ischemia reperfusion injury and pneumonia. Knowledge on the loss or gain of protein expression and activity during disease might tie these enzymes to certain cell types, substrates or interaction partners that are involved in the pathophysiology of the disease, ultimately leading to the elucidation of their functional roles and a potential therapeutic target. Most data could be found on DPP4, while the other enzymes are less explored. Published data however often appear to be conflicting, the applied methods divers and the specificity of the assays used questionable. In conclusion, information on the expression of the proline-specific peptidases in the healthy and diseased lung is lacking, begging for further well-designed research. © Annals of Translational Medicine, 2017. All rights reserved.


Baerts L.,Laboratory of Medical Biochemistry | Gomez N.,University of Sfax | Vanderheyden M.,Cardiovascular Center | De Meester I.,Laboratory of Medical Biochemistry | Mc Entee K.,University of Sfax
Veterinary Journal | Year: 2012

B-type natriuretic peptide or brain natriuretic peptide (BNP) is a cardiac peptide hormone. The principal stimulus for BNP synthesis is myocyte stretch. BNP binds to the natriuretic peptide receptor-A causing increased intracellular cyclic guanosine monophosphate (cGMP) production and shows cardio- and renoprotective effects. However, high endogenous BNP levels are associated with a lack of effect in severe heart failure. Moreover, in experimental heart failure, the response to treatments targeting the natriuretic peptide system is attenuated.This article reviews potential mechanisms that may explain the 'BNP paradox' in heart failure with a focus on interspecies differences, on known and presumed specificities of canine BNP biology, and on experimental studies in dogs. Resistance to BNP is far from fully understood but may be due to post-translational modifications and alteration in proBNP processing, receptor downregulation and desensitization, blunted intracellular signalling and increased clearance of BNP1-32. Alternatively, resistance to BNP may be due to BNP1-32 shortening into additional truncated forms that are less biologically effective. Future improvement in understanding of BNP biology may provide the rationale for innovative therapeutic strategies to maximize cardiovascular and renal cGMP bioavailability. © 2012 Elsevier Ltd.


Gomez N.,University of Sfax | Touihri K.,University of Sfax | Matheeussen V.,Laboratory of Medical Biochemistry | Da Costa A.M.,University of Sfax | And 11 more authors.
European Journal of Heart Failure | Year: 2012

Aims Recent studies indicate that brain natriuretic peptide (BNP 1-32) may be truncated into BNP 3-32 by dipeptidyl peptidase IV (DPP4) and that BNP 3-32 has reduced biological activities compared with BNP 1-32. We investigated if DPP4 contributes to the cardiorenal alterations and to the attenuated response to BNP seen in heart failure. Methods and results Haemodynamic and renal assessment was performed in 12 pigs at baseline, 4 weeks after pacing-induced heart failure, and during BNP infusion. They were randomized to either placebo or treatment with a DPP4 inhibitor, sitagliptin. After 4 weeks of pacing, heart rate was reduced compared with baseline in the sitagliptin group (60 ± 2 vs. 95 ± 16 b.p.m., P < 0.01), and an increase in stroke volume was observed in the sitagliptin group compared with placebo (+24 ± 6% vs.-17 ± 7%, P < 0.01). Glomerular filtration rate declined at week 4 compared with baseline in the placebo group (1.3 ± 0.4 vs. 2.3 ± 0.3 mL/kg/min, P < 0.01) but remained preserved in the sitagliptin group [1.8 ± 0.2 vs. 2.0 ± 0.3 mL/kg/min, P = NS (non-significant)]. In the sitagliptin group, BNP infusion improved end-systolic elastance (68 ± 5 vs. 31 ± 4 mmHg/kg/mL, P < 0.05), ventriculararterial coupling, and mechanical efficiency. Compared with controls (n = 6), myocardial gene expression of BNP, interleukin-6, Na +-Ca 2+ exchanger, and calmodulin was up-regulated in the placebo group, but not in the sitagliptin group. Conclusion In pacing-induced heart failure, DPP4 inhibition preserves the glomerular filtration rate, modulates stroke volume and heart rate, and potentiates the positive inotropic effect of exogenous BNP at no energy expense. © 2011 The Author.


De Schutter S.,Laboratory of Medical Biochemistry | Maertens K.,University of Antwerp | Baerts L.,Laboratory of Medical Biochemistry | De Meester I.,Laboratory of Medical Biochemistry | And 2 more authors.
Pediatric Infectious Disease Journal | Year: 2015

Background: Pertussis vaccination during pregnancy or immediately after delivery is a strategy that is increasingly being recommended to protect young infants from disease. Breast milk contains disease-specific antibodies that can contribute to the protection of young infants. The composition of breast milk could be altered by vaccination during pregnancy or near delivery. However, the quantification of these antibodies in breast milk lacks standardization. Methods: In this paper, sample preparation procedures and detection methods for total and antipertussis toxin (anti-PT) secretory immunoglobulin (sIg) A are proposed that can be accurately repeated and are in accordance with European Medicines Agency and Food and Drug Administration requirements. Both antibody analytes were measured in breast milk samples of lactating women obtained 8-9 weeks postpartum to compare different maternal pertussis vaccination strategies: vaccination during pregnancy, shortly after or at delivery (cocoon), less than 5 years before delivery or more than 5 years before delivery. Results: The validated immunoassays could quantitatively detect total and anti-PT sIgA in the processed breast milk samples. Significantly higher levels of anti-PT sIgA were measured in breast milk after pertussis vaccination during pregnancy or at delivery [geometric mean concentration (GMC): 2.56 and 2.15 IU/mg] in contrast to mothers with no recent (>5 years) pertussis vaccination (GMC: 0.96 IU/mg; P = 0.014 and P = 0.028). Conclusion: Vaccination against pertussis in the second/third trimester of pregnancy or immediately postpartum significantly increased the levels of anti-PT sIgA in breast milk. © 2015 Wolters Kluwer Health, Inc. All rights reserved.


PubMed | Laboratory of Medical Biochemistry
Type: Journal Article | Journal: Veterinary journal (London, England : 1997) | Year: 2012

B-type natriuretic peptide or brain natriuretic peptide (BNP) is a cardiac peptide hormone. The principal stimulus for BNP synthesis is myocyte stretch. BNP binds to the natriuretic peptide receptor-A causing increased intracellular cyclic guanosine monophosphate (cGMP) production and shows cardio- and renoprotective effects. However, high endogenous BNP levels are associated with a lack of effect in severe heart failure. Moreover, in experimental heart failure, the response to treatments targeting the natriuretic peptide system is attenuated. This article reviews potential mechanisms that may explain the BNP paradox in heart failure with a focus on interspecies differences, on known and presumed specificities of canine BNP biology, and on experimental studies in dogs. Resistance to BNP is far from fully understood but may be due to post-translational modifications and alteration in proBNP processing, receptor downregulation and desensitization, blunted intracellular signalling and increased clearance of BNP(1-32.) Alternatively, resistance to BNP may be due to BNP(1-32) shortening into additional truncated forms that are less biologically effective. Future improvement in understanding of BNP biology may provide the rationale for innovative therapeutic strategies to maximize cardiovascular and renal cGMP bioavailability.

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