ISIS AKEMI KATAYAMA RANGEL

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LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina

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Autor: FURUKAWA, Luzia N. S. ×

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  • article 74 Citação(ões) na Scopus
    Inhalation of fine particulate matter during pregnancy increased IL-4 cytokine levels in the fetal portion of the placenta
    (2015) MELO, Juliana Oliveira de; SOTO, Sonia Fatima; KATAYAMA, Isis Akemi; WENCESLAU, Camilla Ferreira; PIRES, Amanda Gonalves; VERAS, Mariana Matera; FURUKAWA, Luzia N. S.; CASTRO, Isac de; SALDIVA, Paulo Hilario Nascimento; HEIMANN, Joel Claudio
    This study aimed to verify the development of placental and systemic inflammation in rats exposed to fine particulate matter before or during pregnancy. Wistar rats were exposed to filtered air ( control) or to a load of 600 mu g/m(3) of fine particles in the air. The gene expression of IL-1 beta, IL-4, IL-6, IL-10, INF-gamma, TNF-alpha and Toll-like receptor 4 in the placenta was evaluated. The serum and placental concentrations of IL-1 beta, IL-4, IL-6, IL-10, INF-gamma and TNF-alpha were measured. The total and differential blood leukocyte and blood platelet count was assessed. Compared to control animals, IL-4 content was elevated in the fetal portion of the placenta in rats exposed to air pollution before and during pregnancy. Increased IL-4 suggests that a placental inflammatory reaction may have occurred in response to exposure to fine particulate matter and that this cytokine was responsible, among possibly others factors, for resolution of the inflammatory reaction.
  • article 26 Citação(ões) na Scopus
    High-Salt Intake Induces Cardiomyocyte Hypertrophy in Rats in Response to Local Angiotensin II Type 1 Receptor Activation
    (2014) KATAYAMA, Isis A.; PEREIRA, Rafael C.; DOPONA, Ellen P. B.; SHIMIZU, Maria H. M.; FURUKAWA, Luzia N. S.; OLIVEIRA, Ivone B.; HEIMANN, Joel C.
    Many studies have shown that risk factors that are independent of blood pressure (BP) can contribute to the development of cardiac hypertrophy (CH). Among these factors, high-salt (HS) intake was prominent. Although some studies have attempted to elucidate the role of salt in the development of this disease, the mechanisms by which salt acts are not yet fully understood. Thus, the aim of this study was to better understand the mechanisms of CH and interstitial fibrosis (IF) caused by HS intake. Male Wistar rats were divided into 5 groups according to diet [normal salt (NS; 1.27% NaCl) or HS (8% NaCl)] and treatment [losartan. (LOS) (HS+LOS group), hydralazine (HZ) (HS+HZ group), or N-acetylcysteine (NAC) (HS+NAC group)], which was given in the drinking water. Tail-cuff BP, transverse diameter of the cardiomyocyte, IF, angiotensin II type 1 receptor (AT1) gene and protein expression, serum aldosterone, cardiac angiotensin II, cardiac thiobarbituric acid-reactive substances, and binding of conformation-specific anti-AT1 and anti-angiotensin II type 2 receptor (AT2) antibodies in the 2 ventricles were measured. Based on the left ventricle transverse diameter data, the primary finding was the occurrence of significant BP-independent CH in the HS+HZ group (96% of the HS group) and a partial or total prevention of such hypertrophy via treatment with NAC or LOS (81% and 67% of the HS group, respectively). The significant total or partial prevention of IF using all 3 treatments (HS+HZ, 27%; HS+LOS, 27%; and HS+NAC, 58% of the HS group, respectively), and an increase in the AT1 gene and protein expression and activity in groups that developed CH, confirmed that CH occurred via the AT1 in this experimental model. Thus, this study unveiled some relevant previously unknown mechanisms of CH induced by chronic HS intake in Wistar rats. The link of oxidative stress with CH in our experimental model is very interesting and stimulates further evaluation for its full comprehension.