RODRIGO RODRIGUES MARCONDES

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LIM/58 - Laboratório de Ginecologia Estrutural e Molecular, Hospital das Clínicas, Faculdade de Medicina

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  • article 8 Citação(ões) na Scopus
    Metoclopramide-induced hyperprolactinemia effects on the pituitary and uterine prolactin receptor expression
    (2013) AMARAL, Vinicius C.; MACIEL, Gustavo A. R.; CARVALHO, Katia C.; MARCONDES, Rodrigo R.; SOARES JR., Jose Maria; BARACAT, Edmund C.
    In this work we have evaluated the gene expression profile of prolactin and prolactin receptor in the pituitary and the uterus of female mice with metoclopramide-induced hyperprolactinemia treated with estrogen and/or progesterone. For this purpose, 49 Swiss female mice were allocated to seven groups. Interventions: 50-day treatment with metoclopramide, progesterone and estrogen. Our results showed that in the pituitary, metoclopramide-induced hyperprolactinemia increased prolactin expression. In the castrated animals, progesterone, with or without estrogen, produced an increase in prolactin. Pituitary prolactin receptor and the estrogen and progesterone treatment were responsible for the rise in PRLR-S2. In the uterus, no differences in prolactin expression were found between the different study groups. PRLR-S1 had its expression reduced in all castrated animals as against the castrated group treated with vehicle. In the noncastrated animals, PRLR-52 rose in the metoclopramide-treated group, and, in the castrated animals, its expression diminished in all groups in relation to the vehicle-treated castrated controls. An increase in PRLR-S3 was found in the oophorectomized animals treated with a combination of estrogen and progesterone. PRLR-L rose in the oophorectomized animals treated with progesterone in isolation or in association with estrogen. These findings suggest that metoclopramide associated to progesterone or estrogen may determine an increase in pituitary prolactin and PRLR-S2 expression. The estrogen-progesterone may enhance the expression of PRLR-S3 and PRLR-L isoform of prolactin receptor.
  • article 7 Citação(ões) na Scopus
    The progesterone and estrogen modify the uterine prolactin and prolactin receptor expression of hyperprolactinemic mice
    (2015) AMARAL, Vinicius Cestari do; CARVALHO, Katia Candido; MACIEL, Gustavo Arantes Rosa; SIMONCINI, Tommaso; SILVA, Priscilla Ludovico da; MARCONDES, Rodrigo Rodrigues; SOARES JR., Jose Maria; BARACAT, Edmund Chada
    The aim of this study was to evaluate the effects of metoclopramide-induced hyperprolactinemia on the prolactin (PRL) and PRL receptor's expression in the uterus of mice. For this purpose, 49 Swiss mice were divided into the following groups: GrSS (non-ovariectomized mice given vehicle); GrMET (non-ovariectomized mice treated with metoclopramide); OvSS (ovariectomized mice given vehicle); OvMET (ovariectomized mice treated with metoclopramide); OvMET+17 beta E (ovariectomized mice treated with metoclopramide and 17 beta estradiol); OvMET+MP (ovariectomized mice treated with metoclopramide and micronized progesterone); OvMET+17 beta E+MP (ovariectomized mice treated with metoclopramide and a solution of 17 beta estradiol and micronized progesterone). Immunohistochemical analyzes were evaluated semi-quantitatively. Our results showed that GrMET, OvMET+MP, and OvMET+17 beta E+MP presented strong PRL expression. OvMET and OvMET+17 beta E presented mild reaction, while GrSS and OvSS presented weak reaction. Concerning PRL receptor, OvMET+MP and OvMET+17 beta E+MP showed strong reaction; GrMET, OvSS, and OvMET+17 beta E showed mild reaction; and GrSS and OvMET showed weak reaction. These findings suggest that progesterone alone or in combination with estrogen may increase the expression of uterine PRL and PRL receptor.
  • article 9 Citação(ões) na Scopus
    Exercise Exercise differentially affects metabolic functions and white adipose tissue in female letrozole-and dihydrotestosterone-induced mouse models of polycystic ovary syndrome
    (2017) MARCONDES, Rodrigo R.; MALIQUEO, Manuel; FORNES, Romina; BENRICK, Anna; HU, Min; IVARSSON, Niklas; CARLSTROM, Mattias; CUSHMAN, Samuel W.; STENKULA, Karin G.; MACIEL, Gustavo A. R.; STENER-VICTORIN, Elisabet
    Here we hypothesized that exercise in dihydrotestosterone (DHT) or letrozole (LET)-induced polycystic ovary syndrome mouse models improves impaired insulin and glucose metabolism, adipose tissue morphology, and expression of genes related to adipogenesis, lipid metabolism, Notch pathway and browning in inguinal and mesenteric fat. DHT-exposed mice had increased body weight, increased number of large mesenteric adipocytes. LET-exposed mice displayed increased body weight and fat mass, decreased insulin sensitivity, increased frequency of small adipocytes and increased expression of genes related to lipolysis in mesenteric fat. In both models, exercise decreased fat mass and inguinal and mesenteric adipose tissue expression of Notch pathway genes, and restored altered mesenteric adipocytes morphology. In conclusion, exercise restored mesenteric adipocytes morphology in DHT- and LET-exposed mice, and insulin sensitivity and mesenteric expression of lipolysis-related genes in LET-exposed mice. Benefits could be explained by downregulation of Notch, and modulation of browning and lipolysis pathways in the adipose tissue.