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33 results on '"Leite, M. Fátima"'

10. CPP-Ts: a new intracellular calcium channel modulator and a promising tool for drug delivery in cancer cells

Author

Oliveira-Mendes, Bárbara Bruna Ribeiro de, Horta, Carolina Campolina Rebello, do Carmo, Anderson Oliveira, Biscoto, Gabriela Lago, Sales-Medina, Douglas Ferreira, Leal, Hortênsia Gomes, Brandão-Dias, Pedro Ferreira Pinto, Miranda, Sued Eustáquio Mendes, Aguiar, Carla Jeane, Cardoso, Valbert Nascimento, de Barros, André Luis Branco, Chávez-Olortégui, Carlos, Leite, M. Fátima, and Kalapothakis, Evanguedes

Published
2018
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15. Nuclear Ca 2+ regulates cardiomyocyte function

Author

Guatimosim, Silvia, Amaya, Maria Jimena, Guerra, Mateus T., Aguiar, Carla J., Goes, Alfredo M., Gómez-Viquez, Norma Leticia, Rodrigues, Michele A., Gomes, Dawidson A., Martins-Cruz, Juliana, Lederer, W.J., and Leite, M. Fatima

Published
2008
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24. Cholesterol-enriched membrane microdomains are needed for insulin signaling and proliferation in hepatic cells

Author

Fonseca, Matheus de Castro, primary, França, Andressa, additional, Florentino, Rodrigo Machado, additional, Fonseca, Roberta Cristelli, additional, Lima Filho, Antônio Carlos Melo, additional, Vidigal, Paula Teixeira Vieira, additional, Oliveira, André Gustavo, additional, Dubuquoy, Laurent, additional, Nathanson, Michael H., additional, and Leite, M. Fátima, additional

Published
2018
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25. Inositol 1, 4, 5-trisphosphate-dependent nuclear calcium signals regulate angiogenesis and cell motility in triple negative breast cancer

Author

Guimarães, Erika, primary, Machado, Rodrigo, additional, Fonseca, Matheus de Castro, additional, França, Andressa, additional, Carvalho, Clarissa, additional, Araújo e Silva, Ana Cândida, additional, Almeida, Brígida, additional, Cassini, Puebla, additional, Hissa, Bárbara, additional, Drumond, Luciana, additional, Gonçalves, Carlos, additional, Fernandes, Gabriel, additional, De Brot, Marina, additional, Moraes, Márcio, additional, Barcelos, Lucíola, additional, Ortega, José Miguel, additional, Oliveira, André, additional, and Leite, M. Fátima, additional

Published
2017
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26. Cholesterol-enriched membrane microdomains are needed for insulin signaling and proliferation in hepatic cells.

Author

de Castro Fonseca, Matheus, França, Andressa, Florentino, Rodrigo Machado, Fonseca, Roberta Cristelli, Lima Filho, Antônio Carlos Melo, Vieira Vidigal, Paula Teixeira, Oliveira, André Gustavo, Dubuquoy, Laurent, Nathanson, Michael H., and Leite, M. Fátima

Subjects
CHOLESTEROL, LIVER cells, INSULIN
Abstract

Hepatocyte proliferation during liver regeneration is a well-coordinated process regulated by the activation of several growth factor receptors, including the insulin receptor (IR). The IR can be localized in part to cholesterol-enriched membrane microdomains, but the role of such domains in insulin-mediated events in hepatocytes is not known. We investigated whether partitioning of IRs into cholesterol-enriched membrane rafts is important for the mitogenic effects of insulin in the hepatic cells. IR and lipid rafts were labeled in HepG2 cells and primary rat hepatocytes. Membrane cholesterol was depleted in vitro with metyl-β-cyclodextrin (MβCD) and in vivo with lovastatin. Insulin-induced calcium (Ca2+) signals studies were examined in HepG2 cells and in freshly isolated rat hepatocytes as well as in whole liver in vivo by intravital confocal imaging. Liver regeneration was studied by 70% partial hepatectomy (PH), and hepatocyte proliferation was assessed by PCNA staining. A subpopulation of IR was found in membrane microdomains enriched in cholesterol. Depletion of cholesterol from plasma membrane resulted in redistribution of the IR along the cells, which was associated with impaired insulin-induced nuclear Ca2+ signals, a signaling event that regulates hepatocyte proliferation. Cholesterol depletion also led to ERK1/2 hyperphosphorylation. Lovastatin administration to rats decreased hepatic cholesterol content, disrupted lipid rafts and decreased insulin-induced Ca2+ signaling in hepatocytes, and delayed liver regeneration after PH. Therefore, membrane cholesterol content and lipid rafts integrity showed to be important for the proliferative effects of insulin in hepatic cells. NEW & NOTEWORTHY One of insulin's actions is to stimulate liver regeneration. Here we show that a subpopulation of insulin receptors is in a specialized cholesterol-enriched region of the cell membrane and this subfraction is important for insulin's proliferative effects. [ABSTRACT FROM AUTHOR]

Published
2018
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28. Inositol 1,4,5-trisphosphate receptor type 3 is involved in resistance to apoptosis and maintenance of human hepatocellular carcinoma.

Author

Dos Santos, Marcone Loiola, França, Andressa, Lima Filho, Antônio Carlos Melo, Florentino, Rodrigo M., Diniz, Paulo Henrique, Oliveira Lemos, Fernanda, Gonçalves, Carlos Alberto Xavier, Coelho, Vitor Lima, Lima, Cristiano Xavier, Foureaux, Giselle, Nathanson, Michael H., Vidigal, Paula Vieira Teixeira, and Leite, M. Fátima

Subjects
HEPATOCELLULAR carcinoma, PROGNOSIS, LIVER cells, INOSITOL, APOPTOSIS, LIVER cancer
Abstract

The expression of the inositol 1,4,5-trisphosphate receptor type 3 (ITRP3) in hepatocytes is a common event in the pathogenesis of hepatocellular carcinoma (HCC), regardless of the type of underlying liver disease. However, it is not known whether ITPR3 expression in hepatocytes is involved in tumor maintenance. The aim of the present study was to determine whether there is an association between ITPR3 expression and clinical and morphological parameters using HCC samples obtained from liver explants from patients (n=53) with different etiologies of underlying chronic liver disease (CLD). ITPR3 expression, mitosis and apoptosis were analyzed in human liver samples by immunohistochemistry. Clinical and event-free survival data were combined to assess the relationship between ITPR3 and liver cancer growth in patients. RNA sequencing analysis was performed to identify apoptotic genes altered by ITPR3 expression in a liver tumor cell line. ITPR3 was highly expressed in HCC tumor cells relative to adjacent CLD tissue and healthy livers. There was an inverse correlation between ITPR3 expression and mitotic and apoptotic indices in HCC, suggesting that ITPR3 contributed to the maintenance of HCC by promoting resistance to apoptosis. This was confirmed by the upregulation of CTSB, CHOP and GADD45, genes involved in the apoptotic pathway in HCC. The expression of ITPR3 in the liver may be a promising prognostic marker of HCC [ABSTRACT FROM AUTHOR]

Published
2022

30. Regulation of Atrial Natriuretic Peptide Secretion by α<SUB>1</SUB>-adrenergic Receptors: The Role of Different Second Messenger Pathways

Author

Ambler, S. Kelly and Leite, M. Fátima

Abstract

A critical problem in determining the intracellular mechanisms regulating atrial natriuretic peptide (ANP) secretion is the extrapolation of data obtained in cultures of atrial myocytes isolated from neonatal animals to that obtained in intact atria isolated from adult animals. We have therefore examined ANP secretory responses in primary cultures of atrial myocytes isolated from adult rats to more closely approach the adult phenotype. Activation of α1-adrenergic receptors by norepinephrine (in the presence of propranolol) increased the rate of ANP secretion approximately two-fold (EC50 = 0.32 µM). This response was mediated predominately by the α1A-like subtype of α1-receptors. Phorbol esters increased the rate of ANP secretion approximately 2.4-fold independently of α1-receptor occupancy. Kinetic analysis showed that the secretory responses to either agonist did not appear to diminish within 2 h. The responses to both α1-adrenergic stimulation and phorbol ester addition were inhibited by the protein kinase C inhibitor, H-7, but not by structurally related isoquinolines. Influx of extracellular CA2+, independently of its effects on contraction of the myocytes, was also necessary for a full secretory response to α1-receptor activation. Additionally, the secretory response to α1-adrenergic agonists was attenuated by calmodulin inhibitors. In contrast to the response to α1-adrenergic receptor activation, stimulation of β-adrenergic receptors or addition of a membrane permeable cAMP analog reduced the rate of both basal and α1-stimulated ANP secretion. These results show that activation of α1-adrenergic receptors in adult rat atrial myocytes directly increases the rate of ANP secretion. This response is dependent upon protein kinase C and supported extracellular Ca2+ influx. Conversely, activation of β-adrenergic receptors, which increases intracellular cAMP, directly inhibits ANP secretion. Copyright 1994, 1999 Academic Press

Published
1994
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