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We studied 22 patients aged 53-78 years scheduled for cardiac surgery under cardiopulmonary bypass. Blood pressure, cardiac output, transcranial Doppler blood flow velocity, arterial blood gases, body temperature and protein S100B, as a marker for cerebral integrity, were evaluated in normotensive and hypertensive patients. Pre-operative mean (SD) arterial blood pressure was 93 (11) mmHg in the normotensive group compared with 116 (15) mmHg in the hypertensive group. We found an increase in protein S100B levels in both groups. Serum protein S100B concentrations in the hypertensive group were significantly higher than in the normotensive group (p < 0.001). The highest mean (SD) values were 2.04 (0.65) micromol x l(-1) in the normotensive group and 7.02 (4.55) micromol x l(-1) in the hypertensive group. These results suggest that cardiopulmonary bypass is associated with a significantly higher rate of cerebral injury in hypertensive patients than in normotensive patients. This may be due to altered autoregulation and insufficient cerebral perfusion. Modifications of cardiopulmonary bypass management for hypertensive patients might be made to decrease the risk of cerebral injury. [ABSTRACT FROM AUTHOR]

Problem: Proper placental development is pivotal to ensure healthy pregnancy outcomes. Among the multiple cellular mechanisms involved in the orchestration of this process, little is known on the role of alternative splicing events in the modulation of trophoblast cell biology. Here, we evaluated the expression of the alternative splicing regulator Rbfox2 in the pre- and post-placentation period in mouse pregnancies in both healthy and pathological settings., Method of Study: Immunofluorescence analysis of Rbfox2 expression in mouse implantation sites collected during the pre-placentation period (E5-E7) and post-placentation (E13)., Results: We identified a progressive increase of Rbfox2 levels throughout the peri-implantation period with a shift from a cytoplasmatic expression on E5-E6 to a predominantly nuclear expression on E7, together with a prominent expression of this factor in both subcellular compartments of the primitive placenta. Our results further showed that in contrast to healthy gestations, Rbfox2 expression decreased in preeclamptic models during the post-placentation period. Finally, we further demonstrated enhanced expression of Rbfox2 proteins in allogeneic pregnancy compared to syngeneic models., Conclusions: Our findings uncover a novel role for Rbfox2-controlled splicing events in the modulation of trophoblast function, with potential implications for the pathogenesis of preeclampsia and other pregnancy complications originated from defective placentation., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Problem: From conception, a delicate regulation of galectins, a family of carbohydrate-binding proteins, is established to ensure maternal immune tolerance in pregnancy. Though galectin-3 (gal-3), the only chimera-type galectin, is abundantly expressed at the feto-maternal interface; the physiological role of this lectin during pregnancy remains to be fully elucidated and requires further investigation., Method of Study: In this study, we analyzed serum gal-3 levels during the course of healthy gestation. Trophoblast functions were evaluated upon gal-3 exogenous stimulation using trophoblastic cell lines (e.g. , HIPEC65, SGHPL-4, and BeWo cells). Finally, we investigated variations in peripheral gal-3 levels associated with the development of spontaneous abortion and gestational diabetes mellitus (GDM)., Results: Gal-3 circulating levels increased as normal pregnancy progressed. In vitro experiments showed that exogenous gal-3 positively regulated trophoblast functions inducing invasion, tube formation, and fusion. Compared with normal pregnant women, circulating gal-3 levels were significantly decreased in patients who developed GDM., Conclusion: Our results reveal a physiological role for gal-3 during pregnancy, promoting proper trophoblast functions associated with healthy gestation. GDM is associated with a failure to increase circulating gal-3 levels late in gestation. Thus, dysregulation of gal-3 may indicate a contribution of the chimera-type lectin to this adverse pregnancy outcome., (© 2020 The Authors. American Journal of Reproductive Immunology published by John Wiley & Sons Ltd.)

Problem: Galectins influence the progress of pregnancy by regulating key processes associated with embryo-maternal cross talk, including angiogenesis and placentation. Galectin family members exert multiple roles in the context of hemochorial and epitheliochorial placentation; however, the galectin prolife in endotheliochorial placenta remains to be investigated., Method of Study: Here, we used immunohistochemistry to analyze galectin (gal)-1, gal-3 and gal-9 expression during early and late endotheliochorial placentation in two different species (dogs and cats)., Results: We found that during early feline gestation, all three galectin members were more strongly expressed on trophoblast and maternal vessels compared to the decidua. This was accompanied by an overall decrease of gal-1, gal-3 and gal-9 expressions in late feline gestation. In canine early pregnancy, we observed that gal-1 and gal-9 were expressed strongly in cytotrophoblast (CTB) cells compared to gal-3, and no galectin expression was observed in syncytiotrophoblast (STB) cells. Progression of canine gestation was accompanied by increased gal-1 and gal-3 expressions on STB cells, whereas gal-9 expression remained similar in CTB and STB., Conclusion: These data suggest that both the maternal and fetal compartments are characterized by a spatiotemporal regulation of galectin expression during endotheliochorial placentation. This strongly suggests the involvement of the galectin family in important developmental processes during gestation including immunemodulation, trophoblast invasion and angiogenesis. A conserved functional role for galectins during mammalian placental development emerges from these studies., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)