MARCIA SILVA QUEIROZ
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- Glutathione peroxidase 4 functional variant rs713041 modulates the risk for cardiovascular autonomic neuropathy in individuals with type 1 diabetes(2019) ADMONI, Sharon Nina; SANTOS-BEZERRA, Daniele Pereira; PEREZ, Ricardo Vesoni; PATENTE, Thiago Andrade; MONTEIRO, Maria Beatriz; CAVALEIRO, Ana Mercedes; PARISI, Maria Candida; NETO, Arnaldo Moura; PAVIN, Elizabeth Joao; QUEIROZ, Marcia Silva; NERY, Marcia; CORREA-GIANNELLA, Maria LuciaCardiac autonomic neuropathy is a neglected diabetic chronic complication for which genetic predictors are rarely reported. Oxidative stress is implicated in the pathogenesis of microvascular complications, and glutathione peroxidase 4 is involved in the detoxification of peroxides and of reactive oxygen species. Thus, the association of a functional variant in the gene encoding glutathione peroxidase 4 (rs713041) with this diabetic complication was investigated in 341 individuals with type 1 diabetes evaluated for cardiac autonomic neuropathy status (61.7% women, 34 [27-42] years old; diabetes duration: 21 [15-27] years; HbA1c: 8.3% [7.4-9.4]; as median [interquartile interval]). Cardiac autonomic neuropathy was present in 29% of the participants. There was an inverse association of the minor T allele of rs713041 with cardiac autonomic neuropathy (odds ratio = 0.39; 95% confidence interval = 0.17-0.90; p = 0.0271) after adjustment for potential confounders. The functional glutathione peroxidase 4 variant rs713041 modulated the risk for cardiac autonomic neuropathy in the studied population with type 1 diabetes.
- Dietary advanced glycated end-products and medicines influence the expression of SIRT1 and DDOST in peripheral mononuclear cells from long-term type 1 diabetes patients(2018) SANTOS-BEZERRA, Daniele P.; MACHADO-LIMA, Adriana; MONTEIRO, Maria Beatriz; ADMONI, Sharon N.; PEREZ, Ricardo V.; MACHADO, Cleide G.; SHIMIZU, Maria Heloiza; CAVALEIRO, Ana M.; THIEME, Karina; QUEIROZ, Marcia S.; MACHADO, Ubiratan F.; GIANNELLA-NETO, Daniel; PASSARELLI, Marisa; CORREA-GIANNELLA, Maria LuciaQuantitative polymerase chain reaction was employed to quantify expression of two genes coding for advanced glycation end-product receptors [RAGE (AGER) and AGER1 (DDOST)] and of the gene coding the deacetylase SIRT1 (SIRT1) in peripheral blood mononuclear cells from type 1 diabetes patients without [Group A, n = 35; 28.5 (24-39) years old; median (interquartile interval)] or with at least one microvascular complication [Group B, n = 117; 34.5 (30-42) years old]; 31 healthy controls were also included. In a subgroup of 48 patients, daily advanced glycation end-products intake before blood collection was assessed. Lower expression of DDOST was found in patients than in controls after adjustment for sex, age, use of statins, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Higher expressions of AGER, DDOST and SIRT1 were observed in Group A. Stratifying by complications, AGER and DDOST expressions were higher in those without retinopathy and without diabetic kidney disease, respectively, compared to patients with these complications. Patients using statins or angiotensin receptor blockers presented higher expression of DDOST. Expression of SIRT1 was higher in patients consuming >= 12,872 KU daily of advanced glycation end-products. Although AGER, DDOST and SIRT1 are differently expressed in peripheral blood mononuclear cells from type 1 diabetes patients with and without microvascular complications, they are also influenced by dietary advanced glycation end-products and by statins and angiotensin receptor blockers.
- Sex-specific associations of variants in regulatory regions of NADPH oxidase-2 (CYBB) and glutathione peroxidase 4 (GPX4) genes with kidney disease in type 1 diabetes(2013) MONTEIRO, M. B.; PATENTE, T. A.; MOHAMMEDI, K.; QUEIROZ, M. S.; AZEVEDO, M. J.; CANANI, L. H.; PARISI, M. C.; MARRE, M.; VELHO, G.; CORREA-GIANNELLA, M. L.Oxidative stress is involved in the pathophysiology of diabetic nephropathy. The superoxide-generating nicotinamide adenine dinucleotide phosphate-oxidase 2 (NOX2, encoded by the CYBB gene) and the antioxidant enzyme glutathione peroxidase 4 (GPX4) play opposing roles in the balance of cellular redox status. In the present study, we investigated associations of single nucleotide polymorphisms (SNPs) in the regulatory regions of CYBB and GPX4 with kidney disease in patients with type 1 diabetes. Two functional SNPs, rs6610650 (CYBB promoter region, chromosome X) and rs713041 (GPX4 3'untranslated region, chromosome 19), were genotyped in 451 patients with type 1 diabetes from a Brazilian cohort (diabetic nephropathy: 44.6%) and in 945 French/Belgian patients with type 1 diabetes from Genesis and GENEDIAB cohorts (diabetic nephropathy: 62.3%). The minor A-allele of CYBB rs6610650 was associated with lower estimated glomerular filtration rate (eGFR) in Brazilian women, and with the prevalence of established/advanced nephropathy in French/Belgian women (odds ratio 1.75, 95% CI 1.11-2.78, p = 0.016). The minor T-allele of GPX4 rs713041 was inversely associated with the prevalence of established/advanced nephropathy in Brazilian men (odds ratio 0.30, 95% CI 0.13-0.68, p = 0.004), and associated with higher eGFR in French/Belgian men. In conclusion, these heterogeneous results suggest that neither CYBB nor GPX4 are major genetic determinants of diabetic nephropathy, but nevertheless, they could modulate in a gender-specific manner the risk for renal disease in patients with type 1 diabetes.
- Thioredoxin interacting protein expression in the urinary sediment associates with renal function decline in type 1 diabetes(2016) MONTEIRO, Maria Beatriz; SANTOS-BEZERRA, Daniele Pereira; THIEME, Karina; ADMONI, Sharon Nina; PEREZ, Ricardo Vessoni; MACHADO, Cleide Guimaraes; QUEIROZ, Marcia Silva; NERY, Marcia; OLIVEIRA-SOUZA, Maria; WORONIK, Viktoria; PASSARELLI, Marisa; GIANNELLA-NETO, Daniel; MACHADO, Ubiratan Fabres; CORREA-GIANNELLA, Maria LuciaAims: Thioredoxin interacting protein (TXNIP), an inhibitor of antioxidant thioredoxin (Trx), is upregulated by hyperglycemia and implicated in pathogenesis of diabetes complications. We evaluated mRNA expressions of genes encoding TXNIP and Trx (TXN) in urinary sediment and peripheral blood mononuclear cells (PBMC) of type 1 diabetes (T1D) patients with different degrees of chronic complications. Methods: qPCR was employed to quantify target genes in urinary sediment (n=55) and PBMC (n=161) from patients sorted by presence or absence of diabetic nephropathy (DN), retinopathy, peripheral and cardiovascular neuropathy; 26 healthy controls and 13 patients presenting non-diabetic nephropathy (focal and segmental glomerulosclerosis, FSGS) were also included. Results: Regarding the urinary sediment, TXNIP (but not TXN) expression was higher in T1D (p=0.0023) and FSGS (p=0.0027) patients versus controls. Expressions of TXNIP and TXN were higher, respectively, in T1D patients with versus without DN (p=0.032) and in those with estimated glomerular filtration rate (eGFR) <60 versus >= 60 mL/min/1.73 m(2) (p=0.008). eGFR negatively correlated with TXNIP (p=0.04, r=-0.28) and TXN (p=0.04, r=-0.30) expressions. T1D patients who lost >= 5 mL/min/1.73 m(2) yearly of eGFR presented higher basal TXNIP expression than those who lost<5 mL/min/1.73 m(2) yearly after median follow-up of 24 months. TXNIP (p<0.0001) and TXN (p=0.002) expressions in PBMC of T1D patients were significantly higher than in controls but no differences were observed between patients with or without chronic complications. Conclusions: TXNIP and TXN are upregulated in urinary sediment of T1D patients with diabetic kidney disease (DKD), but only TXNIP expression is associated with magnitude of eGFR decline.