Browsing by Author "Tichauer, Juan"

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    Pannexin-1 channel opening is critical for COVID-19 pathogenesis
    (CELL PRESS, 2021) Luu, Ross; Valdebenito, Silvana; Scemes, Eliana; Cibelli, Antonio; Spray, David C.; Rovegno, Maximiliano; Tichauer, Juan; Cottignies Calamarte, Andrea; Rosenberg, Arielle; Capron, Calude; Belouzard, Sandrine; Dubuisson, Jean; Annane, Djillali; de la Grandmaison, Geoffroy Lorin; Cramer Borde, Elisabeth; Bomsel, Morgane; Eugenin, Eliseo
    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly rampaged worldwide, causing a pandemic of coronavirus disease (COVID-19), but the biology of SARS-CoV-2 remains under investigation. We demonstrate that both SARS-CoV-2 spike protein and human coronavirus 229E (hCoV-229E) or its purified S protein, one of the main viruses responsible for the common cold, induce the transient opening of Pannexin-1 (Panx-1) channels in human lung epithelial cells. However, the Panx-1 channel opening induced by SARS-CoV-2 is greater and more prolonged than hCoV-229E/S protein, resulting in an enhanced ATP, PGE(2), and IL-1 beta release. Analysis of lung lavages and tissues indicate that Panx-1 mRNA expression is associated with increased ATP, PGE(2), and IL-1 beta levels. Panx-1 channel opening induced by SARS-CoV-2 spike protein is angiotensin-converting enzyme 2 (ACE-2), endocytosis, and furin dependent. Overall, we demonstrated that Panx-1 channel is a critical contributor to SARS-CoV-2 infection and should be considered as an alternative therapy.
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    Proliferating culture of aged microglia for the study of neurodegenerative diseases
    (2011) von Bernhardi, Rommy; Tichauer, Juan; Eugenin-von Bernhardi, Laura
    Microglial cells' phenotype and function change with aging. Since microglial cell impairments that are relevant for neurodegenerative diseases appear to be unique to aged individuals, it is important to assess function of aged microglia. However, most studies are done with microglia from neonates, mostly due to lack of reliable protocols to obtain microglia from adult animals. Here, we present a conditioned media-dependent culture system that promotes proliferation of adult microglia. We observed that inflammatory activation was increasingly oxidative in microglia from aged animals. Also, whereas phagocytosis of A beta by microglia from adult animals was more robust than that of microglia from neonates, the induction of phagocytosis by TGF beta was abolished in aged animals. Our results show the importance of using adult animals cells for the study of neurodegenerative processes or other diseases associated with aging. The proposed culture method is inexpensive and cell yield allows for their assessment by functional bioassays and biochemistry. (C) 2011 Elseviel B.V. All rights reserved.