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RESEARCH PRODUCT
Is Myeloperoxidase a Key Component in the ROS-Induced Vascular Damage Related to Nephropathy in Type 2 Diabetes?
Antonio Hernández-mijaresÁNgeles ÁLvarezAna JoverSusana Rovira-llopisVictor M. VictorRosa FalcónCarmen De PabloMilagros Rochasubject
medicine.medical_specialtyPhysiologyClinical BiochemistryType 2 diabetesmedicine.disease_causeBiochemistryNephropathyProinflammatory cytokinechemistry.chemical_compoundInternal medicinemedicineCell AdhesionHuman Umbilical Vein Endothelial CellsLeukocytesHumansNews & ViewsDiabetic NephropathiesCell adhesionMolecular BiologyCells CulturedGeneral Environmental SciencePeroxidaseCreatininebiologyCell adhesion moleculeCell BiologyMiddle Agedmedicine.diseaseEndocrinologychemistryDiabetes Mellitus Type 2Myeloperoxidasebiology.proteinGeneral Earth and Planetary SciencesCytokinesReactive Oxygen SpeciesCell Adhesion MoleculesOxidative stressdescription
AbstractIt is still unclear whether microvascular complications of type 2 diabetes correlate with leukocyte-endothelium interactions and/or myeloperoxidase (MPO) levels. In the present study, we found that serum levels of glucose, the rate of ROS and MPO concentration were higher in type 2 diabetic patients. Patients with nephropathy (39.6%) presented higher MPO levels that correlate positively with the albumin/creatinine ratio (r=0.59, p<0.05). In addition, nephropatic patients showed increased leukocyte-endothelium interactions due to an undermining of polymorphonuclear leukocytes (PMN) rolling velocity and increased rolling flux and adhesion, which was accompanied by a rise in levels of the proinflammatory cytokine tumour necrosis factor alpha (TNFα) and the adhesion molecule E-selectin. Furthermore, MPO levels were positively correlated with PMN rolling flux (r=0.855, p<0.01) and adhesion (r=0.682, p<0.05). Our results lead to the hypothesis that type 2 diabetes induces oxidative stress and an increase in MPO levels and leukocyte-endothelium interactions, and that these effects correlate with the development of nephropathy. Antioxid. Redox Signal. 19, 1452–1458.
year | journal | country | edition | language |
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2013-11-01 |