Browsing by Author "Brañes, MC"

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    Effect of in vivo administration of epidermal growth factor on prostaglandin production and NOS activity in term rat placentae.: Possible participation of placental EGF receptors
    (2005) Ribeiro, ML; Farina, M; Billi, S; Martínez, SP; Brañes, MC; Villalón, M; Franchi, A
    Many authors hypothesize that the epidermal growth factor (EGF) is involved in the onset of labor. Previous reports from our laboratory showed that intrauterine administration of EGF delays the beginning of labor. The alms of this study were: 1) to analyze the effect of intrauterine administration of 500 ng EGF on placental prostaglandins and nitric oxide, and 2) to characterize the expression of EGF receptors (EGF-R) in pregnant rat placentae. Saline solution (sham group) and 500 ng EGF (EGF-treated group) were administered via intrauterine injection on day 21 of gestation, and both groups of animals were sacrificed on day 22 (sham rats delivered on day 22). Results showed that EGF treatment: 1) inhibited the production of prostaglandin E (p < 0.001) and F-2 alpha (P < 0.01), 2) increased the synthesis of nitric oxide (p < 0.001), and 3) reduced the expression of cyclooxygenase-II, the enzyme responsible for PG synthesis. Placentae were found to express EGF-R and its activated form, and the expressions of both forms were higher at mid and term pregnancy. Hence, EGF is a very interesting molecule for studying the regulation of placental prostaglandin and nitric oxide production related to the parturition process.
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    TNF-α plus IFN-γ induce connexin43 expression and formation of gap junctions between human monocytes/macrophages that enhance physiological responses
    (2003) Eugenín, EA; Brañes, MC; Berman, JW; Sáez, JC
    In this work, the effects of bacterial LPS, TNF-alpha, and IFN-gamma on gap junctional communication (dye coupling) and on the expression of connexin43 (immunofluorescence immunoblotting, and RT-PCR) in monocytes/macrophages were studied. Freshly isolated human monocytes plated at high density and treated either with LPS plus IFN-gamma or TNF-alpha plus IFN-gamma became transiently dye coupled (Lucifer yellow) within 24 h. Cells treated with LPS, TNF-alpha, or IFN-gamma alone remained dye uncoupled. In dye-coupled cells, the spread of Lucifer yellow to neighboring cells was reversibly blocked with 18 alpha-glycyrrhetinic acid, a gap junction blocker, but it was unaffected by oxidized ATP or probenecid, which block ionotropic ATP-activated channels and organic anion transporters, respectively. Abs against TNF-alpha significantly reduced the LPS plus IFN-gamma-induced increase in dye coupling. In dye-coupled monocytes/macrophages, but not in control cells, both connexin43 protein and mRNA were detected, and their levels were higher in cells with an elevated incidence of dye coupling. In dye-coupled cells, the localization of connexin43 immunoreactivity was diffuse at perinuclear regions and thin cell processes. The addition of 18-alpha-glycyrrhetinic acid induced a profound reduction of monocyte/macrophage transmigration across a blood brain barrier model. It also induced a significant reduction in the secretion of metalloproteinase-2 in cells treated with TNF-alpha plus IFN-gamma. We propose that some monocyte/macrophage responses are coordinated by connexin-formed membrane channels expressed transiently at inflammatory sites in which these cells form aggregates.