Marson F.A.L.,University of Campinas |
Ribeiro J.D.,University of Campinas |
Bertuzzo C.S.,University of Campinas |
Salomao Junior J.B.,University of Sao Paulo |
Souza D.R.S.,Research Center for Biochemistry and Molecular Biology
Human Genetics | Year: 2016
The severity of cystic fibrosis (CF) is associated with classes of mutations in the CFTR gene (cystic fibrosis transmembrane regulator), physical environment and modifier genes interaction. The IL8 gene (interleukin 8), according to its respective polymorphisms, influences inflammatory responses. This study analyzed IL8 gene polymorphisms (rs4073, rs2227306 and rs2227307), by means of PCR/RFLP, and their association with pulmonary function markers and clinical severity scores in 186 patients with CF, considering the CFTR genotype. There was an association between rs2227307 and precocity of the disease. The severity of lung disease was associated with the following markers: transcutaneous arterial hemoglobin oxygen saturation (SaO2) (regardless of CFTR genotype, for the polymorphisms rs4073, rs2227306 and rs2227307); mucoid Pseudomonas aeruginosa (regardless of CFTR genotype, for the polymorphisms rs2227306 and rs2227307). Pulmonary function markers (SaO2 and spirometric variables) and clinical severity scores were also associated with IL8 gene polymorphisms. This study identified the IL8 gene, represented by rs4073 and rs2227306 polymorphisms, and particularly the rs2227307 polymorphism, as potentiating factors for the degree of variability in the severity of CF, especially in pulmonary clinical manifestation correlated with increased morbidity and mortality. © 2016 Springer-Verlag Berlin Heidelberg
Qi S.H.,Research Center for Biochemistry and Molecular Biology |
Qi S.H.,Xuzhou Medical College |
Hao L.Y.,Research Center for Biochemistry and Molecular Biology |
Hao L.Y.,Xuzhou Medical College |
And 6 more authors.
Neuropathology and Applied Neurobiology | Year: 2013
Aims: A number of studies have suggested that nitric oxide (NO) plays an important role in the reactive phosphorylation of p38MAPKα (p38). However, whether S-nitrosylation of p38 is activated by NO and the details remain unclear. The aim of the present work was to assess the activation of p38, the S-nitrosylation site and the p38 signalling pathway in rat hippocampus and in HEK293 cell induced by exogenous NO. Methods: Primary hippocampal cultures, HEK293 cells and rat model of cerebral ischaemia/reperfusion (brain ischaemia was induced by four-vessel occlusion procedure) were used in this study. Biotin-switch method and immunoblotting were performed to study the S-nitrosylation and phosphorylation of p38, and neuronal loss was observed by histology. Results: Endogenous NO increased p38 phosphorylation and S-nitrosylation, and the activation of p38 was dependent on the S-nitrosylation of Cys-211, which was critical for the NO-mediated activation of p38. The exogenous NO donor sodium nitroprusside, S-nitrosoglutathione, 7-nitroindazole, the inhibitor of the neuronal nitric oxide synthase, inhibited the activation of p38 signal pathway induced by cerebral ischaemia/reperfusion and attenuated the damage in rat hippocampal neurones. Moreover, the N-methyl-D-aspartate receptor (NMDAR) is probably involved in the p38 activation process of S-nitrosylation and phosphorylation. Conclusion: Endogenous NO induces the S-nitrosylation and phosphorylation of p38 and mediates p38 signalling pathway by NMDAR, and as exogenous NO inhibits this process and is neuroprotective in rat cerebral ischaemia/reperfusion, it may make a contribution to stroke therapy. © 2012 The Authors. Neuropathology and Applied Neurobiology © 2012 British Neuropathological Society.
Baitello M.E.L.,Research Center for Biochemistry and Molecular Biology |
Tenani G.D.,Research Center for Biochemistry and Molecular Biology |
Ferreira R.F.,Research Center for Biochemistry and Molecular Biology |
Nogueira V.,Research Center for Biochemistry and Molecular Biology |
And 6 more authors.
Canadian Journal of Gastroenterology and Hepatology | Year: 2016
Hepatocellular carcinoma (HCC) is the most common primary neoplasia of the liver. Major risk factors for hepatocellular carcinoma include chronic liver diseases, carcinogenic agents, and genetic alterations as well as vascular endothelial growth factor (VEGF) involved in angiogenesis process. The aim of this study was to evaluate the association of VEGF-A (C936T and A1154G) with HCC and cirrhosis, in addition to serum levels of VEGF, clinical profile, lifestyle habits, and comorbidities. A total of 346 individuals were studied: 102 with HCC (G1), 117 with cirrhosis (G2), and 127 controls (G3). Polymorphisms were analysed by PCR/RFLP and serum levels of VEGF by ELISA. Alpha error was set at 5%. The wild-type genotype of both polymorphisms prevailed (P > 0.05). In G1, 23% of the patients died, with no relation to genetic profile (P > 0.05). Increased VEGF level was observed in G1 and G3, related to the mutant allele of VEGF-C936T and VEGF-A1154G, respectively, and compared with the wild-type genotype (P = 0.0285; P = 0.0284, resp.) as well as G1 versus G2 and G3 for VEGF-C936T and G1 versus G2 for VEGF-A1154G (P < 0.05 for both). In conclusion, there is a relationship between mutant alleles of VEGF-C936T and VEGF-A1154G polymorphisms and higher VEGF level, making them potential markers for HCC. © 2016 Maria Eduarda Lopes Baitello et al.
PubMed | Research Center for Biochemistry and Molecular Biology and University Medical Center
Type: | Journal: Canadian journal of gastroenterology & hepatology | Year: 2016
Hepatocellular carcinoma (HCC) is the most common primary neoplasia of the liver. Major risk factors for hepatocellular carcinoma include chronic liver diseases, carcinogenic agents, and genetic alterations as well as vascular endothelial growth factor (VEGF) involved in angiogenesis process. The aim of this study was to evaluate the association of