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RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ

Microglia, the main resident immune cells in the CNS, are thought to participate in the pathogenesis of various neurological disorders. LPS and LPS + IFNγ are stimuli that are widely used to activate microglia. However, the transcriptomic profiles of microglia treated with LPS and LPS + IFNγ have no...

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Autores principales: Pulido-Salgado, Marta, Vidal-Taboada, Jose M., Barriga, Gerardo Garcia-Diaz, Solà, Carme, Saura, Josep
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208373/
https://www.ncbi.nlm.nih.gov/pubmed/30382133
http://dx.doi.org/10.1038/s41598-018-34412-9
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author Pulido-Salgado, Marta
Vidal-Taboada, Jose M.
Barriga, Gerardo Garcia-Diaz
Solà, Carme
Saura, Josep
author_facet Pulido-Salgado, Marta
Vidal-Taboada, Jose M.
Barriga, Gerardo Garcia-Diaz
Solà, Carme
Saura, Josep
author_sort Pulido-Salgado, Marta
collection PubMed
description Microglia, the main resident immune cells in the CNS, are thought to participate in the pathogenesis of various neurological disorders. LPS and LPS + IFNγ are stimuli that are widely used to activate microglia. However, the transcriptomic profiles of microglia treated with LPS and LPS + IFNγ have not been properly compared. Here, we treated murine primary microglial cultures with LPS or LPS + IFNγ for 6 hours and then performed RNA-Sequencing. Gene expression patterns induced by the treatments were obtained by WGCNA and 11 different expression profiles were found, showing differential responses to LPS and LPS + IFNγ in many genes. Interestingly, a subset of genes involved in Parkinson’s, Alzheimer’s and Huntington’s disease were downregulated by both treatments. By DESeq analysis we found differentially upregulated and downregulated genes that confirmed LPS and LPS + IFNγ as inducers of microglial pro-inflammatory responses, but also highlighted their involvement in specific cell functions. In response to LPS, microglia tended to be more proliferative, pro-inflammatory and phagocytic; whereas LPS + IFNγ inhibited genes were involved in pain, cell division and, unexpectedly, production of some inflammatory mediators. In summary, this study provides a detailed description of the transcriptome of LPS- and LPS + IFNγ treated primary microglial cultures. It may be useful to determine whether these in vitro phenotypes resemble microglia in in vivo pathological conditions.
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spelling pubmed-62083732018-11-01 RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ Pulido-Salgado, Marta Vidal-Taboada, Jose M. Barriga, Gerardo Garcia-Diaz Solà, Carme Saura, Josep Sci Rep Article Microglia, the main resident immune cells in the CNS, are thought to participate in the pathogenesis of various neurological disorders. LPS and LPS + IFNγ are stimuli that are widely used to activate microglia. However, the transcriptomic profiles of microglia treated with LPS and LPS + IFNγ have not been properly compared. Here, we treated murine primary microglial cultures with LPS or LPS + IFNγ for 6 hours and then performed RNA-Sequencing. Gene expression patterns induced by the treatments were obtained by WGCNA and 11 different expression profiles were found, showing differential responses to LPS and LPS + IFNγ in many genes. Interestingly, a subset of genes involved in Parkinson’s, Alzheimer’s and Huntington’s disease were downregulated by both treatments. By DESeq analysis we found differentially upregulated and downregulated genes that confirmed LPS and LPS + IFNγ as inducers of microglial pro-inflammatory responses, but also highlighted their involvement in specific cell functions. In response to LPS, microglia tended to be more proliferative, pro-inflammatory and phagocytic; whereas LPS + IFNγ inhibited genes were involved in pain, cell division and, unexpectedly, production of some inflammatory mediators. In summary, this study provides a detailed description of the transcriptome of LPS- and LPS + IFNγ treated primary microglial cultures. It may be useful to determine whether these in vitro phenotypes resemble microglia in in vivo pathological conditions. Nature Publishing Group UK 2018-10-31 /pmc/articles/PMC6208373/ /pubmed/30382133 http://dx.doi.org/10.1038/s41598-018-34412-9 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Pulido-Salgado, Marta
Vidal-Taboada, Jose M.
Barriga, Gerardo Garcia-Diaz
Solà, Carme
Saura, Josep
RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ
title RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ
title_full RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ
title_fullStr RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ
title_full_unstemmed RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ
title_short RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ
title_sort rna-seq transcriptomic profiling of primary murine microglia treated with lps or lps + ifnγ
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208373/
https://www.ncbi.nlm.nih.gov/pubmed/30382133
http://dx.doi.org/10.1038/s41598-018-34412-9
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