QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.

<h4>Background</h4>The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein. This gene was shown to be essential for myelination in oligodendrocytes. QKI is also highly expressed in astrocytes, but it...

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Autores principales: Lin Jiang, Peter Saetre, Katarzyna J Radomska, Elena Jazin, Eva Lindholm Carlström
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Publicado: Public Library of Science (PLoS) 2010
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spelling oai:doaj.org-article:5731ee0d823345e5a308daa7c60dc01a2021-11-18T07:03:51ZQKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.1932-620310.1371/journal.pone.0013079https://doaj.org/article/5731ee0d823345e5a308daa7c60dc01a2010-09-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20927331/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein. This gene was shown to be essential for myelination in oligodendrocytes. QKI is also highly expressed in astrocytes, but its function in these cells is not known.<h4>Methods/principal findings</h4>We studied the effect of small interference RNA (siRNA)-mediated QKI depletion on global gene expression in human astrocyte glioma cells. Microarray measurements were confirmed with real-time quantitative polymerase chain reaction (qPCR). The presence of QKI binding sites (QRE) was assessed by a bioinformatic approach. Viability and cell morphology were also studied. The most significant alteration after QKI silencing was the decreased expression of genes involved in interferon (IFN) induction (P = 6.3E-10), including IFIT1, IFIT2, MX1, MX2, G1P2, G1P3, GBP1 and IFIH1. All eight genes were down-regulated after silencing of the splice variant QKI-7, but were not affected by QKI-5 silencing. Interestingly, four of them were up-regulated after treatment with the antipsychotic agent haloperidol that also resulted in increased QKI-7 mRNA levels.<h4>Conclusions/significance</h4>The coordinated expression of QKI-7 splice variant and IFN-related genes supports the idea that this particular splice variant has specific functions in astrocytes. Furthermore, a role of QKI-7 as a regulator of an inflammatory gene pathway in astrocytes is suggested. This hypothesis is well in line with growing experimental evidence on the role of inflammatory components in schizophrenia.Lin JiangPeter SaetreKatarzyna J RadomskaElena JazinEva Lindholm CarlströmPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 9 (2010)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Lin Jiang
Peter Saetre
Katarzyna J Radomska
Elena Jazin
Eva Lindholm Carlström
QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
description <h4>Background</h4>The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein. This gene was shown to be essential for myelination in oligodendrocytes. QKI is also highly expressed in astrocytes, but its function in these cells is not known.<h4>Methods/principal findings</h4>We studied the effect of small interference RNA (siRNA)-mediated QKI depletion on global gene expression in human astrocyte glioma cells. Microarray measurements were confirmed with real-time quantitative polymerase chain reaction (qPCR). The presence of QKI binding sites (QRE) was assessed by a bioinformatic approach. Viability and cell morphology were also studied. The most significant alteration after QKI silencing was the decreased expression of genes involved in interferon (IFN) induction (P = 6.3E-10), including IFIT1, IFIT2, MX1, MX2, G1P2, G1P3, GBP1 and IFIH1. All eight genes were down-regulated after silencing of the splice variant QKI-7, but were not affected by QKI-5 silencing. Interestingly, four of them were up-regulated after treatment with the antipsychotic agent haloperidol that also resulted in increased QKI-7 mRNA levels.<h4>Conclusions/significance</h4>The coordinated expression of QKI-7 splice variant and IFN-related genes supports the idea that this particular splice variant has specific functions in astrocytes. Furthermore, a role of QKI-7 as a regulator of an inflammatory gene pathway in astrocytes is suggested. This hypothesis is well in line with growing experimental evidence on the role of inflammatory components in schizophrenia.
format article
author Lin Jiang
Peter Saetre
Katarzyna J Radomska
Elena Jazin
Eva Lindholm Carlström
author_facet Lin Jiang
Peter Saetre
Katarzyna J Radomska
Elena Jazin
Eva Lindholm Carlström
author_sort Lin Jiang
title QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
title_short QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
title_full QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
title_fullStr QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
title_full_unstemmed QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
title_sort qki-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/5731ee0d823345e5a308daa7c60dc01a
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AT elenajazin qki7regulatesexpressionofinterferonrelatedgenesinhumanastrocytegliomacells
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