Alpha 2 Na+,K+-ATPase silencing induces loss of inflammatory response and ouabain protection in glial cells

التفاصيل البيبلوغرافية
العنوان: Alpha 2 Na+,K+-ATPase silencing induces loss of inflammatory response and ouabain protection in glial cells
المؤلفون: Cristoforo Scavone, Ana Maria Marques Orellana, Larissa de Sá Lima, L. M. Yshii, Elisa Mitiko Kawamoto, Paula Fernanda Kinoshita, Amanda Galvão Paixão, Andrea Rodrigues Vasconcelos
المصدر: Scientific Reports
Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
Scientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
بيانات النشر: Nature Publishing Group UK, 2017.
سنة النشر: 2017
مصطلحات موضوعية: 0301 basic medicine, MAPK/ERK pathway, Lipopolysaccharides, Science, Biology, FARMACOLOGIA, Models, Biological, Ouabain, Article, 03 medical and health sciences, Mice, medicine, Animals, Viability assay, Gene Silencing, Na+/K+-ATPase, Enzyme Inhibitors, Cells, Cultured, Cardiac glycoside, G alpha subunit, Inflammation, Multidisciplinary, respiratory system, Cell biology, 030104 developmental biology, Neuroprotective Agents, Cell culture, Medicine, Signal transduction, Sodium-Potassium-Exchanging ATPase, Neuroglia, medicine.drug
الوصف: Ouabain (OUA) is a cardiac glycoside that binds to Na+,K+-ATPase (NKA), a conserved membrane protein that controls cell transmembrane ionic concentrations and requires ATP hydrolysis. At nM concentrations, OUA activates signaling pathways that are not related to its typical inhibitory effect on the NKA pump. Activation of these signaling pathways protects against some types of injury of the kidneys and central nervous system. There are 4 isoforms of the alpha subunit of NKA, which are differentially distributed across tissues and may have different physiological roles. Glial cells are important regulators of injury and inflammation in the brain and express the α1 and α2 NKA isoforms. This study investigated the role of α2 NKA in OUA modulation of the neuroinflammatory response induced by lipopolysaccharide (LPS) in mouse primary glial cell cultures. LPS treatment increased lactate dehydrogenase release, while OUA did not decrease cell viability and blocked LPS-induced NF-κB activation. Silencing α2 NKA prevented ERK and NF-κB activation by LPS. α2 NKA also regulates TNF-α and IL-1β levels. The data reported here indicate a significant role of α2 NKA in regulating central LPS effects, with implications in the associated neuroinflammatory processes.
اللغة: English
تدمد: 2045-2322
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2317d0a9413c3508001f14b63103c1e8Test
http://europepmc.org/articles/PMC5501845Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....2317d0a9413c3508001f14b63103c1e8
قاعدة البيانات: OpenAIRE