ISIS AKEMI KATAYAMA RANGEL

(Fonte: Lattes)
Índice h a partir de 2011
3
Projetos de Pesquisa
Unidades Organizacionais
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina

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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 8 Citação(ões) na Scopus
    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.