ISIS AKEMI KATAYAMA RANGEL
Projetos de Pesquisa
Unidades Organizacionais
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina
8 resultados
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conferenceObject Myocardial AT1 gene expression is increased in a model of left ventricular hypertrophy induced by high salt intake(2013) PEREIRA, Rafael Canavel; KATAYAMA, Isis Akemi; HEIMANN, Joel ClaudioObjective: To evaluate gene expression of the renin-angiotensin system components in a model of left ventricular hypertrophy induced by high salt intake demonstrated in a previous study. Methods: Wistar rats were fed normal (NS1.3% NaCl) or high (HS 8%) salt diet since weaning. From the 7th week of age, two HS subgroups received hydralazine or losartan (HZ 15 and LOS 20mg/kg/day). Angiotensinogen, renin, ACE, ACE2, AT1 and AT2 gene expression in left ventricle were measured. Data are reported as mean±SEM. Means in row with superscripts without a common letter differ, P<0.05. Conclusion: High salt intake increases AT1 gene expression, however it is prevented by losartan treatment.conferenceObject Lysine Specific Demethylase-1 Deficiency Accelerates the Development of Hypertension and Renal Damage During Long Term Sodium Intake(2019) KATAYAMA, Isis Akemi; CULLINANE, Danielle L.; WILLIAMS, Gordon H.; HEIMANN, Joel Claudio; POJOGA, Luminita H.conferenceObject Male Mice Heterozygous LSD1 Knockout Gene Prevented the Effect of High Sodium Intake on Renal Fibrosis and AT1 Conformational Status(2019) NASCIMENTO, Mariana Moura; KATAYAMA, Isis Akemi; POJOGA, Luminita H.; HEIMANN, Joel Claudio- 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 ClaudioThis 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.
- 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.
- Histone demethylase LSD1 deficiency and biological sex: impact on blood pressure and aldosterone production(2019) HUANG, Yuefei; TING, Pei Yee; YAO, Tham M.; HOMMA, Tsuyoshi; BROOKS, Danielle; RANGEL, Isis Katayama; ADLER, Gail K.; ROMERO, Jose R.; WILLIAMS, Jonathan S.; POJOGA, Luminita H.; WILLIAMS, Gordon H.Human risk allele carriers of lysine-specific demethylase 1 (LSD1) and LSD1-deficient mice have salt-sensitive hypertension for unclear reasons. We hypothesized that LSD1 deficiency causes dysregulation of aldosterone's response to salt intake resulting in increased cardiovascular risk factors (blood pressure and microalbumin). Furthermore, we determined the effect of biological sex on these potential abnormalities. To test our hypotheses, LSD1 male and female heterozygote-knockout (LSD1+/-) and WT mice were assigned to two age groups: 18 weeks and 36 weeks. Plasma aldosterone levels and aldosterone production from zona glomerulosa cells studied ex vivo were greater in both male and female LSD1+/- mice consuming a liberal salt diet as compared to WT mice consuming the same diet. However, salt-sensitive blood pressure elevation and increased microalbuminuria were only observed in male LSD1+/- mice. These data suggest that LSD1 interacts with aldosterone's secretory response to salt intake. Lack of LSD1 causes inappropriate aldosterone production on a liberal salt diet; males appear to be more sensitive to this aldosterone increase as males, but not females, develop salt sensitivity of blood pressure and increased microalbuminuria. The mechanism responsible for the cardiovascular protective effect in females is uncertain but may be related to estrogen modulating the effect of mineralocorticoid receptor activation.
conferenceObject Salt induced cardiac hypertrophy is blood pressure independent and prevented by Losartan and N-acetylcysteine(2013) KATAYAMA, Isis Akemi; PEREIRA, Rafael Canavel; SHIMIZU, Maria Heloisa Massola; HEIMANN, Joel ClaudioconferenceObject Mechanisms of myocardial alterations induced by chronic high-salt intake(2012) KATAYAMA, Isis Akemi; DOPONA, Ellen Priscila Brito; HEIMANN, Joel Claudio