Effects of repetitive transcranial magnetic stimulation on ER stress-related genes and glutamate, γ-aminobutyric acid and glycine transporter genes in mouse brain.

Repetitive transcranial magnetic stimulation (rTMS) is an emerging therapy for the treatment of psychiatric disorders. However, the mechanisms underlying the therapeutic effects of rTMS are still unclear, limiting its optimisation. Lasting effects suggest changes in disease-related genes, so we conducted gene chip and qRT-PCR analyses of genes associated with psychiatric diseases in the mouse brain at various times following 1, 20, 30 or 40 days of rTMS.

Gene expression microarray data from mouse CBS treated with rTMS for 30 days, mouse cerebrum and CBS treated with rTMS for 40 days.

This data article contains complementary tables related to the research article study entitled, 'Effects of repetitive transcranial magnetic stimulation on ER stress-related genes and glutamate, γ-aminobutyric acid, and glycine transporter genes in mouse brain' (Ikeda et al. (2017) [1]), which showed that rTMS modulates glutamate, GABA and glycine transporters and regulates ER stress-related genes. Here, we provide accompanying data collected using Affymetrix GeneChip microarrays to identify changes in gene expression in mouse CBS treated with rTMS for 30 days (Tables 1-21) and mouse cerebrum (Tables 22-57) and CBS (Tables 58-94) treated with rTMS for 40 days.

Gene expression microarray data from mouse cerebrum treated with rTMS for 30 days.

This data article contains complementary tables related to the research article entitled, 'Effects of repetitive transcranial magnetic stimulation on ER stress-related genes and glutamate, γ-aminobutyric acid, and glycine transporter genes in mouse brain' (Ikeda et al. (2017) [1]), which showed that rTMS modulates glutamate, GABA and glycine transporters and regulates ER stress-related genes. Here we provide accompanying data collected using Affymetrix GeneChip microarrays to identify changes in gene expression in mouse cerebrum treated with rTMS for 30 days (Tables 1-10).

Data on CUX1 isoforms in idiopathic pulmonary fibrosis lung and systemic sclerosis skin tissue sections.

This data article contains complementary figures related to the research article entitled, "Transforming growth factor-β-induced CUX1 isoforms are associated with fibrosis in systemic sclerosis lung fibroblasts" (Ikeda et al. (2016) [2], http://dx.doi.

Transforming growth factor--induced CUX1 isoforms are associated with fibrosis in systemic sclerosis lung fibroblasts.

In the enhancer region of the human type I collagen alpha 2 () gene, we identified cis-elements for the transcription factor CUX1. However, the role of CUX1 in fibrosis remains unclear. Here we investigated the role of CUX1 in the regulation of COL1 expression and delineated the mechanisms underlying the regulation of expression by CUX1 in systemic sclerosis (SSc) lung fibroblasts.

Soluble CD26/Dipeptidyl Peptidase IV Enhances the Transcription of IL-6 and TNF-α in THP-1 Cells and Monocytes.

CD26 is a 110-kDa multifunctional molecule having dipeptidyl peptidase IV (DPPIV) enzyme activity and is present on the surface of human T cells. Soluble CD26 (sCD26) exists in human blood and enhances the proliferation of peripheral T lymphocytes induced by tetanus toxoid (TT). The mechanisms by which CD26 enhances the activation of T cells and monocytes remain to be fully elucidated.

Multiple effects of repetitive transcranial magnetic stimulation on neuropsychiatric disorders.

Repetitive transcranial magnetic stimulation (rTMS) is a new tool that has been used for the treatment of patients with neuropsychiatric disorders. However, the mechanisms underlying the effects of rTMS are still unclear. We analyzed the changes in mRNA expression in mouse brain that occurred after rTMS with an Affymetrix GeneChip.

High doses of TGF-β potently suppress type I collagen via the transcription factor CUX1.

Transforming growth factor-β (TGF-β) is an inducer of type I collagen, and uncontrolled collagen production leads to tissue scarring and organ failure. Here we hypothesize that uncovering a molecular mechanism that enables us to switch off type I collagen may prove beneficial in treating fibrosis. For the first time, to our knowledge, we provide evidence that CUX1 acts as a negative regulator of TGF-β and potent inhibitor of type I collagen transcription.

Halogenation of 4-hydroxy-3-methoxybenzyl thiourea TRPV1 agonists showed enhanced antagonism to capsaicin.

Selected potent TRPV1 agonists (1-6) have been modified by 5- or 6-halogenation on the aromatic A-region to analyze their effects on potency and efficacy (agonism versus antagonism). The halogenation caused enhanced functional antagonism at TRPV1 compared to the corresponding prototype agonists. The analysis of SAR indicated that the antagonism was enhanced as the size of the halogen increased (I>Br>Cl) and when the 6-position was halogenated.

Sodium channel beta4 subunit: down-regulation and possible involvement in neuritic degeneration in Huntington's disease transgenic mice.

Sodium channel beta4 is a very recently identified auxiliary subunit of the voltage-gated sodium channels. To find the primarily affected gene in Huntington's disease (HD) pathogenesis, we profiled HD transgenic mice using a high-density oligonucleotide array and identified beta4 as an expressed sequence tag (EST) that was significantly down-regulated in the striatum of HD model mice and patients. Reduction in beta4 started at a presymptomatic stage in HD mice, whereas other voltage-gated ion channel subunits were decreased later.

Modulation of monoamine transporter expression and function by repetitive transcranial magnetic stimulation.

Repetitive transcranial magnetic stimulation (rTMS) is a new tool for the treatment of neuropsychiatric disorders. However, the mechanisms underlying the effects of rTMS are still unclear. In this study, we analyzed mRNA expression changes of monoamine transporter (MAT) genes, which are targets for antidepressants and psychostimulants.

Trehalose alleviates polyglutamine-mediated pathology in a mouse model of Huntington disease.

Inhibition of polyglutamine-induced protein aggregation could provide treatment options for polyglutamine diseases such as Huntington disease. Here we showed through in vitro screening studies that various disaccharides can inhibit polyglutamine-mediated protein aggregation. We also found that various disaccharides reduced polyglutamine aggregates and increased survival in a cellular model of Huntington disease.