Association study of myelin transcription factor 1‐like polymorphisms with schizophrenia in Han Chinese population

Li, W.; Wang, Xiaopo; Zhao, Jian; Lin, Jianghai; Song, Xueqin; Yang, Yongfeng; Jiang, Chengdi; Xiao, Bo; Yang, Ge; Zhang, H.-X.; Lv, Luxian

doi:10.1111/j.1601-183x.2011.00734.x

Cited by 29 publications

(26 citation statements)

References 53 publications

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“…MYT1L is essential to neurogenesis and differentiating neurons in the mammalian brain (Kim et al 1997;Nielsen et al 2004;Vierbuchen et al 2010). Genetic variants and copy-number variants in the this gene have been associated with SCZ (Vrijenhoek et al 2008;Lee et al 2012;Li et al 2012;Van Den Bossche et al 2013). There are several limitations to this study.…”

Section: Discussionmentioning

confidence: 99%

Aberrant DNA Methylation of Blood in Schizophrenia by Adjusting for Estimated Cellular Proportions

et al. 2014

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DNA methylation, which is the transference of a methyl group to the 5'-carbon position of the cytosine in a CpG dinucleotide, is one of the major mechanisms of epigenetic modifications. A number of studies have demonstrated altered DNA methylation of peripheral blood cells in schizophrenia (SCZ) in previous studies. However, most of these studies have been limited to the analysis of the CpG sites in CpG islands in gene promoter regions, and cell-type proportions of peripheral leukocytes, which may be one of the potential confounding factors for DNA methylation, have not been adjusted in these studies. In this study, we performed a genome-wide DNA methylation profiling of the peripheral leukocytes from patients with SCZ and from non-psychiatric controls (N = 105; 63 SCZ and 42 control subjects) using a quantitative high-resolution DNA methylation microarray which covered across the whole gene region (485,764 CpG dinucleotides). In the DNA methylation data analysis, we first estimated the cell-type proportions of each sample with a published algorithm. Next, we performed a surrogate variable analysis to identify potential confounding factors in our microarray data. Finally, we conducted a multiple linear regression analysis in consideration of these factors, including estimated cell-type proportions, and identified aberrant DNA methylation in SCZ at 2,552 CpG loci at a 5% false discovery rate correction. Our results suggest that altered DNA methylation may be involved in the pathophysiology of SCZ, and cell heterogeneity adjustments may be necessary for DNA methylation analysis.

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Section: Discussionmentioning

confidence: 99%

Aberrant DNA Methylation of Blood in Schizophrenia by Adjusting for Estimated Cellular Proportions

et al. 2014

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“…All data in italics are statistically significant genes such as ZNF804A (Zhang et al 2011a), the myelin transcription factor 1-like (MYT1L) (Li et al 2012), the synapse-associated protein 97 gene (SAP97) (Uezato et al 2012), disrupted-in-schizophrenia-1 (DISC1) (Schumacher et al 2009), reelin (RELN) (Shifman et al 2008), and interferon γ (IFN-γ) (Paul-Samojedny et al 2011). …”

Section: Discussionmentioning

confidence: 99%

Heat shock protein 70 gene polymorphisms are associated with paranoid schizophrenia in the Polish population

Kowalczyk

Owczarek

Suchanek

et al. 2014

Cell Stress and Chaperones

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HSP70 genes have been considered as promising schizophrenia candidate genes based on their protective role in the central nervous system under stress conditions. In this study, we analyzed the potential implication of HSPA1A +190G/C, HSPA1B +1267A/G, and HSPA1L +2437T/C polymorphisms in the susceptibility to paranoid schizophrenia in a homogenous Caucasian Polish population. In addition, we investigated the association of the polymorphisms with the clinical variables of the disease. Two hundred and three patients with paranoid schizophrenia and 243 healthy controls were enrolled in the study. Polymorphisms of HSPA1A, -1B, and -1L genes were genotyped using the PCR-RFLP technique. Analyses were conducted in entire groups and in subgroups that were stratified according to gender. There were significant differences in the genotype and allele frequencies of HSPA1A polymorphism between the patients and controls. The +190CC genotype and +190C allele were overrepresented in the patients and significantly increased the risk for developing schizophrenia (OR=3.45 and OR=1.61, respectively). Interestingly, such a risk was higher for females with the +190CC genotype than for males with the +190CC genotype (OR=5.78 vs. OR=2.76). We also identified the CGT haplotype as a risk haplotype for schizophrenia and demonstrated the effects of HSPA1A and HSPA1B genotypes on the psychopathology and age of onset. Our study provided the first evidence that the HSPA1A polymorphism may potentially increase the risk of developing paranoid schizophrenia. Further independent analyses in different populations to evaluate the role of gender are needed to replicate these results.

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“…Additional signaling co-factors such as With No Lysine K (WNK1) 25 , Myelin transcription factor 1 (Myt1) and its homolog Myt1-like (Myt1l) are known to be associated with Lingo-1 signaling due to a lack of p75 and TROY receptors on Lingo-1 expressing neurons 26,27 . Genetic associations with schizophrenia have been previously reported for the Myt1l gene in different populations 28,29 , and the knockdown of Myt1 has been shown to induce apoptosis 30 , strengthening the relevance of studying this Lingo-1 cofactor in a neurodevelopmental PCP induced model for schizophrenia.…”

Section: Introductionmentioning

confidence: 96%

Alterations of p75 neurotrophin receptor and Myelin transcription factor 1 in the hippocampus of perinatal phencyclidine treated rats

Andrews

Newell

Matosin

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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(2015). Alterations of p75 neurotrophin receptor and Myelin transcription factor 1 in the hippocampus of perinatal phencyclidine treated rats. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 63 91-97.Alterations of p75 neurotrophin receptor and Myelin transcription factor 1 in the hippocampus of perinatal phencyclidine treated rats AbstractPostnatal administration of phencyclidine (PCP) in rodents causes major disturbances to neurological processes resulting in severe modifications to normal behavioral traits into adulthood. It is routinely used to model psychiatric disorders such as schizophrenia, producing many of the dysfunctional processes in the brain that are present in this devastating disorder, including elevated levels of apoptosis during neurodevelopment and disruptions to myelin and plasticity processes. Lingo-1 (or Leucine-rich repeat and immunoglobulin domain-containing protein) is responsible for negatively regulating neurite outgrowth and the myelination of axons. Recent findings using a postmortem human brain cohort showed that Lingo-1 signaling partners in the Nogo receptor (NgR)/p75/TNF receptor orphan Y (TROY) signaling complex, and downstream signaling partners With No Lysine (K) (WNK1) and Myelin transcription factor 1 (Myt1), play a significant part in schizophrenia pathophysiology. Here we have examined the implication of Lingo-1 and its signaling partners in a neurodevelopmental model of schizophrenia using PCP to determine if these pathways are altered in the hippocampus throughout different stages of neurodevelopment. Male Sprague-Dawley rats were injected subcutaneously with PCP (10 mg/kg) or saline solution on postnatal days (PN) 7, 9, and 11. Rats (n = 6/group) were sacrificed at PN12, 5 weeks, or 14 weeks. Relative expression levels of Lingo-1 signaling proteins were examined in the hippocampus of the treated rats. p75 and Myt1 were decreased (0.001 ≤ p ≤ 0.011) in the PCP treated rats at PN12. There were no significant changes in any of the tested proteins at 5 weeks (p > 0.05). At 14 weeks, p75, TROY, and Myt1 were increased in the PCP treated rats (0.014 ≤ p ≤ 0.022). This is the first report of an alteration in Lingo-1 signaling proteins in the rat hippocampus, both directly after PCP treatment in early development and in adulthood. Based on our results, we propose that components of the Lingo-1 signaling pathways may be involved in the acute neurotoxicity induced by perinatal administration of PCP in rats early in development and suggest that this may have implications for the hippocampal deficits seen in schizophrenia. Male Sprague Dawley rats were injected subcutaneously with PCP (10mg/kg) or saline solution on postnatal days (PN)7, 9 and 11. Rats (n=6/group) were sacrificed at PN12, 5 weeks or 14 weeks. Relative expression levels of Lingo-1 signaling proteins were examined in the hippocampus of the treated rats. p75 and Myt1 were decreased (0.001≤p≤0.011) in the PCP treated rats at PN12. There were no significant changes in any of the tested proteins at 5 we...

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Association study of myelin transcription factor 1‐like polymorphisms with schizophrenia in Han Chinese population

Cited by 29 publications

References 53 publications

Aberrant DNA Methylation of Blood in Schizophrenia by Adjusting for Estimated Cellular Proportions

Aberrant DNA Methylation of Blood in Schizophrenia by Adjusting for Estimated Cellular Proportions

Heat shock protein 70 gene polymorphisms are associated with paranoid schizophrenia in the Polish population

Alterations of p75 neurotrophin receptor and Myelin transcription factor 1 in the hippocampus of perinatal phencyclidine treated rats

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