Identification of suitable reference genes for BDV-infected primary rat hippocampal neurons

Mao, Qiang; Zhang, Lujun; Guo, Yujie; Sun, Lu; Liu, Siwen; He, Peng; Huang, Rongzhong; Sun, Lin; Chen, Shigang; Zhang, Hong

doi:10.3892/mmr.2016.5959

Cited by 7 publications

(7 citation statements)

References 36 publications

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“…The symptoms are similar to human cognitive and emotional disorders. 33 In this study, SD rats infected with BoDV-1 had a longer escape latency, crossed the platform fewer times, and spent less time in the target quadrant. The results indicated that newborn rats infected with BoDV-1 developed cognitive impairment as adults.…”

Section: Bodv-1 Upregulates Tlr4 Myd88 and Irf5 Expression In The Rat Hippocampusmentioning

confidence: 62%

BoDV‐1 infection induces neuroinflammation by activating the TLR4/MyD88/IRF5 signaling pathway, leading to learning and memory impairment in rats

Tang

Guo

et al. 2021

Journal of Medical Virology

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Borna disease virus (BoDV-1) can infect the hippocampus and limbic lobes of newborn rodents, causing cognitive deficits and abnormal behavior. Studies have found that neuroinflammation caused by viral infection in early life can affect brain development and impair learning and memory function, revealing the important role of neuroinflammation in cognitive impairment caused by viral infection. However, there is no research to explore the pathogenic mechanism of BoDV-1 in cognition from the direction of neuroinflammation. We established a BoDV-1 infection model in rats, and tested the learning and memory impairment by Morris water maze (MWM) experiment. RNAseq was introduced to detect changes in the gene expression profile of BoDV-1 infection, focusing on inflammation factors and related signaling pathways. BoDV-1 infection impairs the learning and memory of Sprague-Dawley rats in the MWM test and increases the expression of inflammatory cytokines in the hippocampus. RNAseq analysis found 986 differentially expressed genes (DEGs), of which 845 genes were upregulated and 141 genes were downregulated, and 28 genes were found to be enriched in the toll-like receptor (TLR) pathway. The expression of TLR4, MyD88, and IRF5 in the hippocampus was significantly changed in the BoDV-1 group. Our results indicate that BoDV-1 infection stimulates TLR4/ MyD88/IRF5 pathway activation, causing the release of downstream inflammatory factors, which leads to neuroinflammation in rats. Neuroinflammation may play a significant role in learning and memory impairment caused by BoDV-1 infection.

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Section: Bodv-1 Upregulates Tlr4 Myd88 and Irf5 Expression In The Rat Hippocampusmentioning

confidence: 62%

BoDV‐1 infection induces neuroinflammation by activating the TLR4/MyD88/IRF5 signaling pathway, leading to learning and memory impairment in rats

Tang

Guo

et al. 2021

Journal of Medical Virology

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“…BoDV-1-infection may induce a large spectrum of neurological disorders ranging from immune-mediated acute encephalitis to non-inflammatory behavioral alterations [7,8]. Previous studies demonstrated that BoDV-1 establishes a persistent infection in the hippocampus and limbic lobe of rodents in the neonatal period, which induced cognitive deficits and mental disorders [4,9]. Notwithstanding abundant discussion of BoDV-1-driven pathophysiology, the precise mechanism underlying how BoDV-1 disrupts memory is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Jie

Xia

et al. 2018

Cell Physiol Biochem

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Background/Aims: Borna disease virus 1 (BoDV-1) infection induces cognitive impairment in rodents. Emerging evidence has demonstrated that Chromatin remodeling through histone acetylation can regulate cognitive function. In the present study, we investigated the epigenetic regulation of chromatin that underlies BoDV-1-induced cognitive changes in the hippocampus. Methods: Immunofluorescence assay was applied to detect BoDV-1 infection in hippocampal neurons and Sprague-Dawley rats models. The histone acetylation levels both in vivo and vitro were assessed by western blots. The acetylation-regulated genes were identified by ChIP-seq and verified by RT-qPCR. Cognitive functions were evaluated with Morris Water Maze test. In addition, Golgi staining, and electrophysiology were used to study changes in synaptic structure and function. Results: BoDV-1 infection of hippocampal neurons significantly decreased H3K9 histone acetylation level and inhibited transcription of several synaptic genes, including postsynaptic density 95 (PSD95) and brain-derived neurotrophic factor (BDNF). Furthermore, BoDV-1 infection of Sprague Dawley rats disrupted synaptic plasticity and caused spatial memory impairment. These rats also exhibited dysregulated hippocampal H3K9 acetylation and decreased PSD95 and BDNF protein expression. Treatment with the HDAC inhibitor, suberanilohydroxamic acid (SAHA), attenuated the negative effects of BoDV-1. Conclusion: Our results demonstrate that regulation of H3K9 histone acetylation may play an important role in BoDV-1-induced memory impairment, whereas SAHA may confer protection against BoDV-1-induced cognitive impairments. This study finds important

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“…(microRNA 101a). However, this was considered by the final ranking as the most stable reference gene (Mao et al, 2016). With this in mind, the creation of RefFinder is justified, aiming to acquire information of greater validity.…”

Section: Discussionmentioning

confidence: 99%

Validation of reference genes for RT-qPCR in cardiac tissue of rats induced to obesity and diabetes

Oliveira

Livramento

Magalhães

et al. 2020

RSD

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The validation of reference genes is an essential step for any RT-qPCR analysis. In this way, the present paper aimed to identify and validate reference genes for RT-qPCR in cardiac tissue of rats of the Rattus norvegicus albinus specie, submitted to obesity associated or not to type 2 diabetes mellitus. For this, the metabolic changes were induced at the 42nd day of life and the euthanasia was performed on the 70th day. The heart apexes were collected and destinates for RNA extraction. The RT-qPCR technique was performed in own thermocycler, the efficiency of the primers found by the LinReg software and the stability of the expression of the reference genes in the samples was analyzed by the RefFinder algorithm. The candidates for reference genes were GAPDH, POLR2A, RPL32, and RPL4 and the target gene used to verify the differences in gene expression of candidates for reference genes was CMA1. The obese animals showed a decrease in CMA1 gene expression when compared to the two most stable reference genes. The opposite occurs when it is compared to the two less stable reference genes. The GAPDH and POLR2A genes are the best to normalize the reactions with the samples in question. There is no universal reference gene for all situations, which requires systematic validation for each situation. The use of unvalidated reference genes may compromise the interpretation of the expression of the target genes, which would prevent the reflection of the actual situation.

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Identification of suitable reference genes for BDV-infected primary rat hippocampal neurons

Cited by 7 publications

References 36 publications

BoDV‐1 infection induces neuroinflammation by activating the TLR4/MyD88/IRF5 signaling pathway, leading to learning and memory impairment in rats

BoDV‐1 infection induces neuroinflammation by activating the TLR4/MyD88/IRF5 signaling pathway, leading to learning and memory impairment in rats

Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation

Validation of reference genes for RT-qPCR in cardiac tissue of rats induced to obesity and diabetes

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