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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Kinoshita, Paula F. ; Yshii, Lidia M. ; Orellana, Ana Maria M. ; Paixao, Amanda G. ; Vasconcelos, Andrea R. ; Lima, Larissa De Sa ; Kawamoto, Elisa M. ; Scavone, Cristoforo
Total Authors: 8
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 7, JUL 7 2017.
Web of Science Citations: 2
Abstract

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 alpha 1 and alpha 2 NKA isoforms. This study investigated the role of alpha 2 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-kappa B activation. Silencing alpha 2 NKA prevented ERK and NF-kappa B activation by LPS. alpha 2 NKA also regulates TNF-alpha and IL-1 beta levels. The data reported here indicate a significant role of alpha 2 NKA in regulating central LPS effects, with implications in the associated neuroinflammatory processes. (AU)

FAPESP's process: 11/22844-0 - Study of the molecular mechanism activation of Wnt/Beta Catenin Signaling pathway by Ouabain in rat hippocampus.
Grantee:Ana Maria Marques Orellana
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 11/10303-5 - TRAF6 and alfa-synuclein interaction and the subsequent modulation of signaling pathways
Grantee:Lidia Mitiko Yshii
Support Opportunities: Scholarships in Brazil - Post-Doctoral
FAPESP's process: 14/05026-0 - Effects of ouabain in memory and in response to stress: influence of Na, K-ATPase in the modulation of NF-kB / CREB- Wnt -BDNF glucocorticoids and / corticotropin signaling cascades in the central nervous system
Grantee:Cristoforo Scavone
Support Opportunities: Regular Research Grants
FAPESP's process: 16/07376-4 - Evaluation of the effects of PTEN compartmentalization in human cells of glioblastoma (U87MG) submitted to a inflammatory stimuli
Grantee:Amanda Galvão da Paixão
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 11/21308-8 - Evaluation of PTEN compartmentalization on neurogenesis and synaptic plasticity influenced by environmental factors
Grantee:Elisa Mitiko Kawamoto Iwashe
Support Opportunities: Research Grants - Young Investigators Grants
FAPESP's process: 11/12255-8 - Influence of TLR4 receptors in behavioral and neurochemical alterations caused by intermittent fasting in C3H/HeJ mice
Grantee:Andrea Rodrigues Vasconcelos
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 11/04327-9 - Changes in LPS induced gene expression by ouabain signaling on alpha1, alpha2 Na, K-ATPase in glial cells
Grantee:Paula Fernanda Kinoshita
Support Opportunities: Scholarships in Brazil - Master