Browsing by Author "Yuseff, Maria Isabel"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
- ItemAntibody to AP1B adaptor blocks biosynthetic and recycling routes of basolateral proteins at recycling endosomes(AMER SOC CELL BIOLOGY, 2007) Cancino, Jorge; Torrealba, Carolina; Soza, Andrea; Yuseff, Maria Isabel; Gravotta, Diego; Henklein, Peter; Rodriguez Boulan, Enrique; Gonzalez, AlfonsoThe epithelial-specific adaptor AP1B sorts basolateral plasma membrane (PM) proteins in both biosynthetic and recycling routes, but the site where it carries out this function remains incompletely defined. Here, we have investigated this topic in Fischer rat thyroid (FRT) epithelial cells using an antibody against the medium subunit mu 1B. This antibody was suitable for immunofluorescence and blocked the function of AP1B in these cells. The antibody blocked the basolateral recycling of two basolateral PM markers, Transferrin receptor (TfR) and LDL receptor (LDLR), in a perinuclear compartment with marker and functional characteristics of recycling endosomes (RE). Live imaging experiments demonstrated that in the presence of the antibody two newly synthesized GFP-tagged basolateral proteins (vesicular stomatitis virus G [VSVG] protein and TfR) exited the trans-Golgi network (TGN) normally but became blocked at the RE within 3-5 min. By contrast, the antibody did not block trafficking of green fluorescent protein (GFP)-LDLR from the TGN to the PM but stopped its recycling after internalization into RE in similar to 45 min. Our experiments conclusively demonstrate that 1) AP1B functions exclusively at RE; 2) TGN-to-RE transport is very fast and selective and is mediated by adaptors different from AP1B; and 3) the TGN and AP1B-containing RE cooperate in biosynthetic basolateral sorting.
- ItemClinical and pulmonary function analysis in long-COVID revealed that long-term pulmonary dysfunction is associated with vascular inflammation pathways and metabolic syndrome(FRONTIERS MEDIA SA, 2023) Sanhueza, Sergio; Vidal, Mabel A.; Hernandez, Mauricio A.; Henriquez-Beltran, Mario E.; Cabrera, Camilo; Quiroga, Romina; Antilef, Barbara E.; Aguilar, Kevin P.; Castillo, Daniela A.; Llerena, Faryd J.; Figueroa, Marco Fraga; Nazal, Mauricio; Castro, Eritson; Lagos, Paola; Moreno, Alexa; Lastra, Jaime J.; Gajardo, Jorge; Garces, Pamela; Riffo, Benilde; Buchert, Jorge; Sanhueza, Rocio; Ormazaba, Valeska; Saldivia, Pablo; Vargas, Cristian; Nourdin, Guillermo; Koch, Elard; Zuniga, Felipe A.; Lamperti, Liliana; Bustos, Paula; Guzman-Gutierrez, Enrique; Tapia, Claudio A.; Ferrada, Luciano; Cerda, Gustavo; Woehlbier, Ute; Riquelme, Marcelo; Yuseff, Maria Isabel; Ramirez, Braulio A. Munoz; Lombardi, Giovanna; De Gonzalo-Calvo, David; Salomon, Carlos; Verdugo, Ricardo A.; Quinones, Luis A.; Colombo, Alicia; Barria, Maria I.; Labarca, Gonzalo; Nova-Lamperti, EstefaniaIntroduction: Long-term pulmonary dysfunction (L-TPD) is one of the most critical manifestations of long-COVID. This lung affection has been associated with disease severity during the acute phase and the presence of previous comorbidities, however, the clinical manifestations, the concomitant consequences and the molecular pathways supporting this clinical condition remain unknown. The aim of this study was to identify and characterize L-TPD in patients with long-COVID and elucidate the main pathways and long-term consequences attributed to this condition by analyzing clinical parameters and functional tests supported by machine learning and serum proteome profiling. Methods: Patients with L-TPD were classified according to the results of their computer-tomography (CT) scan and diffusing capacity of the lungs for carbon monoxide adjusted for hemoglobin (DLCOc) tests at 4 and 12-months post-infection. Results: Regarding the acute phase, our data showed that L-TPD was favored in elderly patients with hypertension or insulin resistance, supported by pathways associated with vascular inflammation and chemotaxis of phagocytes, according to computer proteomics. Then, at 4-months post-infection, clinical and functional tests revealed that L-TPD patients exhibited a restrictive lung condition, impaired aerobic capacity and reduced muscular strength. At this time point, high circulating levels of platelets and CXCL9, and an inhibited FCgamma-receptor-mediated-phagocytosis due to reduced Fc gamma RIII (CD16) expression in CD14+ monocytes was observed in patients with L-TPD. Finally, 1-year post infection, patients with L-TPD worsened metabolic syndrome and augmented body mass index in comparison with other patient groups. Discussion: Overall, our data demonstrated that CT scan and DLCOc identified patients with L-TPD after COVID-19. This condition was associated with vascular inflammation and impair phagocytosis of virus-antibody immune complexes by reduced Fc gamma RIII expression. In addition, we conclude that COVID-19 survivors required a personalized follow-up and adequate intervention to reduce long-term sequelae and the appearance of further metabolic diseases.