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Introducción: La diabetes mellitus gestacional se manifiesta con una intolerancia a los carbohidratos, ocasionada por una alteración en la secreción de insulina, con descontrol de los niveles de glucosa en sangre, caracterizada por ser una condición temporal y que se desarrolla por primera vez durante el embarazo; suele desaparecer después del parto, pero puede desarrollarse diabetes mellitus en un futuro. Metodología: Se realizó un estudio investigativo tipo documental, sistematizada, descriptiva, prospectiva en un periodo de revisión de cinco años, del 2013 a 2018. Discusión: Entre los trastornos más comunes en el feto esta la macrostomia, posterior al nacimiento se puede desarrollar hipoglu-cemia. Por parte de la madre también se han documentado complicaciones que pueden percutir al momento del parto como la preeclampsia y el síndrome metabólico. Conclusiones: La diabetes gestacional puede cursar asintomática, por lo que se recomienda realizar pruebas de medición de glucosa en sangre durante las semanas 24 y 28 de gestación. Hay factores que pueden incrementar los riesgos de desarrollar diabetes gestacional, como: la edad avanzada de la madre, sobrepeso u obesidad, antecedentes familiares de diabetes mellitus, entre otros. Por lo tanto, someterse a la prueba de tamizaje sigue siendo el método más seguro de detección.

Introduction: Gestational diabetes mellitus manifests itself with a carbohydrate intolerance, caused by an alteration in insulin secretion, with uncontrolled blood glucose levels, characterized by being a temporary condition, which develops for the first time during pregnancy; It usually disappears after childbirth, although diabetes mellitus may develop later. Methodology: A documentary, systematic, descriptive, prospective research study was conducted in a five-year review period, from 2013 to 2018. Discussion: Among the most common disorders in the fetus is macrostomia, hypoglycemia may develop after birth. On the part of the mother complications have also been documented that can affect the moment of delivery such as preeclampsia and metabolic syndrome. Conclusions:Gestational diabetes can be asymptomatic, so it is recommended to perform blood glucose measu-rement tests during weeks 24 and 28 of gestation. There are factors that can increase the risks of developing gestational diabetes, such as: the mother's advanced age, overweight or obesity, family history of diabetes mellitus, among others. Therefore, undergoing the screening test remains the safest method of detection

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In this study, we analyzed soluble factors secreted by two Estrogen Receptor Positive (ER-α) human breast cancer cell lines, ZR 75.30 (luminal B) and MCF7 (luminal A), and evaluated their effect on endothelial activation. The composition of tumoral soluble factors (TSFs) was analyzed by ELISA (Bio-Plex). TSFs from ZR 75.30 cells expressed higher levels of TNF, IFN-γ, IL-6, and IL-8 compared to TSFs from MCF-7 cells. TSFs from ZR 75.30 cells induced a pro-adhesive phenotype in human umbilical vein endothelial cells (HUVECs), as characterized by increased monocytic cell adhesion, adhesion molecule expression and NF-κB activation and decreased IκB-α expression. Conversely, TSFs from MCF-7 cells exerted none of these effects on HUVECs. We then added TNF, IFN-γ, IL-6 or IL-8 alone or in combination with TSFs from MCF-7 cells to HUVECs. Only the combinations that included TNF induced endothelial activation. A neutralizing antibody against IL-1ß (this cytokine was not measured in the ELISA) had a modest blocking effect on cellular adhesion or the expression of adhesion molecules induced by TSFs from ZR 75.30 cells in HUVECs. However neutralizing antibodies against TNF, IFN-γ, IL-6 or IL-8 had no effect. Our results suggest that although TNF is an inducer of endothelial cell activation, it is not the only molecule that is responsible for this effect in TSFs from ZR 75.30 cells.

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Rho guanine nucleotide exchange factors (RhoGEFs) integrate cell signaling inputs into morphological and functional responses. However, little is known about the endothelial repertoire of RhoGEFs and their regulation. Thus, we assessed the expression of 81 RhoGEFs (70 homologous to Dbl and 11 of the DOCK family) in endothelial cells. Further, in the case of DH-RhoGEFs, we also determined their responses to VEGF exposure in vitro and in the context of tumors. A phylogenetic analysis revealed the existence of four groups of DH-RhoGEFs and two of the DOCK family. Among them, we found that the most abundant endothelial RhoGEFs were: Tuba, FGD5, Farp1, ARHGEF17, TRIO, P-Rex1, ARHGEF15, ARHGEF11, ABR, Farp2, ARHGEF40, ALS, DOCK1, DOCK7 and DOCK6. Expression of RASGRF2 and PREX2 increased significantly in response to VEGF, but most other RhoGEFs were unaffected. Interestingly murine endothelial cells isolated from tumors showed that all four phylogenetic subgroups of DH-RhoGEFs were altered when compared to non-tumor endothelial cells. In summary, our results provide a detailed assessment of RhoGEFs expression profiles in the endothelium and set the basis to systematically address their regulation in vascular signaling.

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Calcium-sensing receptor (CaR) activates intracellular pathways controlling calcium homeostasis. CaR carboxyl-terminal mutants associated with metabolic diseases suggest that unidentified proteins interact with the carboxyl-terminal region of this receptor. To address this possibility, we screened for CaR-interacting proteins using the carboxyl terminus of CaR (CaRDelta895-1075 deletion mutant). We identified AMSH, an ubiquitin isopeptidase, as a CaR-interacting partner. AMSH caused a decrease on the signaling properties of wild-type and mutant CaR. Our results indicate that AMSH, which has been recently characterized as a regulator of the endosomal sorting of epidermal growth factor receptor, represents a novel modulator of CaR signaling.

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