PRISCILLA LUDOVICO DA SILVA
Projetos de Pesquisa
Unidades Organizacionais
LIM/58 - Laboratório de Ginecologia Estrutural e Molecular, Hospital das Clínicas, Faculdade de Medicina
7 resultados
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conferenceObject Cytoskeleton remodeling and migration of T47D breast cancer cell enhanced by prolactin(2016) SILVA, Priscilla Da; AMARAL, Vinicius Do; BARACAT, Edmund; SOARES- JR., Jose Maria; SIMONCINI, Tommaso- Effects of hyperprolactinemia on the tibial epiphyseal plate of mice treated with sex hormones(2016) WOLFF, Roberta B.; GOMES, Regina Celia T.; AMARAL, Vinicius C. do; SILVA, Priscilla L. da; SIMONCINI, Tommaso; PROSDOCIMI, Fabio Cesar; SIMOES, Ricardo S.; SIMOES, Manuel Jesus S.; BARACAT, Edmund C.; SOARES JR., Jose MariaThe aim of this study was to evaluate the effects of metoclopramide-induced hyperprolactinemia on the tibial epiphyseal plate of hormone-treated oophorectomized mice. For this purpose, 18 animals with intact ovaries were allocated to two groups, M (metoclopramide) and V (vehicle). One hundred and eight oophorectomized animals were allocated to 12 subgroups: Oophx/V (vehicle); Ooph/M (metoclopramide); Oophx/V+E (vehicle+estradiol); Oophx/M+E (metoclopramide+estradiol); Oophx/V+P (vehicle+progesterone); Oophx/M+P (metoclopramide+progesterone); Oophx/V+T (vehicle+testosterone); Oophx/M+T (metoclopramide+testosterone); Oophx/V+E+P (Vehicle+estradiol+progesterone); Oophx/M+E+P (metoclopramide+estradiol+progesterone); Oophx/V+E+P+T (vehicle+estradiol+progesterone+testosterone); Oophx/M+E+P+T (metoclopramide+estradiol+progesterone+testosterone). After a 50-day treatment was performed histomorphometric and immunohistochemical cell death analysis. In the epiphyseal plate of the hyperprolactinemic and/or oophorectomized animals, cell proliferation and bone formation decreased, inducing intensified cell death. In the sex steroid-treated animals, estrogen boosted cell proliferation; progesterone, bone formation and testosterone, both cell proliferation and bone formation. These findings suggest that oophorectomy and hyperprolactinemia changed epiphyseal plate morphology causing cartilage degeneration. Treatment with combined sex steroids may diminish such deleterious effects.
- 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 ChadaThe 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.
conferenceObject Estrogen enhances glucose transporter 4 and insulin substrate 1 expressions in SGBS-adipocyte submitted to low and high glucose concentration(2016) AMARAL, Vinicius Do; SOARES- JR., Jose Maria; SILVA, Priscilla Da; BARACAT, Edmund; SIMONCINI, Tommaso- Effects of metoclopramide-induced hyperprolactinemia on the prolactin and prolactin receptor expression of murine adrenal(2015) AMARAL, Vinicius Cestari do; SILVA, Priscilla Ludovico da; CARVALHO, Katia Candido; SIMONCINI, Tommaso; MACIEL, Gustavo Arantes Rosa; SOARES- JR., Jose Maria; BARACAT, Edmund ChadaThe aim of this study was to evaluate the effects of metoclopramide-induced hyperprolactinemia on the prolactin (PRL) and prolactin receptor's (PRLR) expression in the adrenal. For this purpose, a total of 12 animals with intact ovaries were allocated to two groups: G1 (saline solution) and G2 (metoclopramide). A total of 30 oophorectomized animals was randomized to five subgroups: G3 (saline solution), G4 (metoclopramide), G5 (metoclopramide + 17 beta-estradiol), G6 (metoclopramide + progesterone), and G7 (metoclopramide + 17 beta-estradiol + progesterone). Immunohistochemical analyses were evaluated semi-quantitatively. For PRLR, the area fraction of labeled cells (ALC) varied from 1 (0-10%) to 3 (> 50%). Based on the mean of the immunostaining intensity, G2 and G4 showed strong expression; G6 and G7 presented a mild reaction; and G1, G3, and G5 exhibited a weak reaction. Concerning PRL, the ALC varied from 1 (0-10%) to 3 (> 50%), and groups G6 and G7 showed a strong reaction; G2, G4, and G5 showed a mild reaction; and G1 and G3 exhibited a weak reaction. These findings suggest that metoclopramide-induced hyperprolactinemia increases PRL expression in the adrenal glands of mice. Furthermore, progesterone alone or in association with estrogen also increases PRL expression, but to a lesser extent.
- Prolactin Promotes Breast Cancer Cell Migration through Actin Cytoskeleton Remodeling(2015) SILVA, Priscilla Ludovico da; AMARAL, Vinicius Cestari do; GABRIELLI, Valentina; GUEVARA, Maria Magdalena Montt; MANNELLA, Paolo; BARACAT, Edmund Chada; SOARES- JR., Jose Maria; SIMONCINI, TommasoThe role of prolactin on breast cancer development and progression is debated. Breast cancer progression largely depends on cell movement and on the ability to remodel the actin cytoskeleton. In this process, actin-binding proteins are requested to achieve fibrillar actin de-polymerization and relocation at the cell membrane. Kinases such as focal adhesion kinase (FAK) are later required to form actin/vinculin-enriched structures called focal adhesion complexes, which mediate firm adhesion to the extracellular matrix. These controllers are regulated by c-Src, which forms multiprotein signaling complexes with membrane receptors and is regulated by a number of hormones, including prolactin. We here show that breast cancer cells exposed to prolactin display an elevated c-Src expression and phosphorylation. In parallel, increased moesin and FAK expression and phosphorylation are found. These molecular changes are associated to relocation to the plasma membrane of cytoskeletal actin fibers and to increased horizontal cell movement. In conclusion, prolactin regulates actin remodeling and enhances breast cancer cell movement. This finding broadens the understanding of prolactin actions on breast cancer cells, highlighting new pathways that may be relevant to on breast cancer progression.
conferenceObject Prolactin and prolactin receptor expression on the adrenal of hyperprolactinemic mice treated with estrogen and progesterone(2016) AMARAL, Vinicius Do; SILVA, Priscilla Da; CARVALHO, Katia; SIMONCINI, Tommaso; MACIEL, Gustavo Arantes; SOARES- JR., Jose Maria; BARACAT, Edmund