Imbalance between hippocampal projection cell and parvalbumin interneuron architecture increases epileptic susceptibility in mouse model of methyl CpG binding protein 2 duplication syndrome.

Objective: Methyl CpG-binding protein 2 (MECP2) duplication syndrome is a rare X-linked genomic disorder affecting predominantly males, which is usually manifested as epilepsy and autism spectrum disorder (ASD) comorbidity. The transgenic line MeCP2 was used for mimicking MECP2 duplication syndrome and showed autism-epilepsy co-occurrence. Previous works suggested that the excitatory/inhibitory (E/I) imbalance is a potential common mechanism for both epilepsy and ASD.

Mitochondrial DNA damage triggers spread of Parkinson's disease-like pathology.

In the field of neurodegenerative diseases, especially sporadic Parkinson's disease (sPD) with dementia (sPDD), the question of how the disease starts and spreads in the brain remains central. While prion-like proteins have been designated as a culprit, recent studies suggest the involvement of additional factors. We found that oxidative stress, damaged DNA binding, cytosolic DNA sensing, and Toll-Like Receptor (TLR)4/9 activation pathways are strongly associated with the sPDD transcriptome, which has dysregulated type I Interferon (IFN) signaling.

Integrative Proteome Analysis Revels 3-Hydroxybutyrate Exerts Neuroprotective Effect by Influencing Chromatin Bivalency.

3-hydroxybutyrate (3OHB) has been proved to act as a neuroprotective molecule in multiple neurodegenerative diseases. Here, we employed a quantitative proteomics approach to assess the changes of the global protein expression pattern of neural cells upon 3OHB administration. In combination with a disease-related, protein-protein interaction network we pinpointed a hub marker, histone lysine 27 trimethylation, which is one of the key epigenetic markers in multiple neurodegenerative diseases.

Excitatory and Inhibitory Synaptic Imbalance Caused by Brain-Derived Neurotrophic Factor Deficits During Development in a Valproic Acid Mouse Model of Autism.

Environmental factors, such as medication during pregnancy, are one of the major causes of autism spectrum disorder (ASD). Valproic acid (VPA) intake during pregnancy has been reported to dramatically elevate autism risk in offspring. Recently, researchers have proposed that VPA exposure could induce excitatory or inhibitory synaptic dysfunction.

Continuous wave irradiation at 0.1 terahertz facilitates transmembrane transport of small molecules.

The bioeffects of terahertz (THz) radiation received growing attention because of its influence on the interactions between biomolecules. Our work aimed to investigate the effects of THz irradiation on cell membrane, especially cell membrane permeability. We found that 0.

PIAS2-mediated blockade of IFN-β signaling: a basis for sporadic Parkinson disease dementia.

Familial Parkinson disease (PD) is associated with rare genetic mutations, but the etiology in most patients with sporadic (s)PD is largely unknown, and the basis for its progression to dementia (sPDD) is poorly characterized. We have identified that loss of IFNβ or IFNAR1, the receptor for IFNα/β, causes pathological and behavioral changes resembling PDD, prompting us to hypothesize that dysregulated genes in IFNβ-IFNAR signaling pathway predispose one to sPD. By transcriptomic analysis, we found defective neuronal IFNβ-IFNAR signaling, including particularly elevated PIAS2 associated with sPDD.

0.1 THz exposure affects primary hippocampus neuron gene expression via alternating transcription factor binding.

In recent years, many studies have been conducted to investigate the influence of terahertz (THz) radiation on the gene expression in various cell types, but the underling molecular mechanism has not yet been fully revealed. In this study, we explored the effects of 0.1 THz radiation on the gene expression in primary neuron cells through RNA-seq analysis.

Beta-Hydroxybutyrate Enhances BDNF Expression by Increasing H3K4me3 and Decreasing H2AK119ub in Hippocampal Neurons.

Neurological evidence suggests that beta-hydroxybutyrate (BHBA) has positive effects on the central nervous system. Previous studies have explored the molecular mechanisms by which BHBA affects different brain functions, but the effects of BHBA on epigenetic modifications remain elusive. Here, we showed that BHBA enhanced brain-derived neurotrophic factor (BDNF) expression by increasing H3K4me3 and decreasing H2AK119ub occupancy at the promoters I, II, IV, and VI in hippocampal neurons.

Study of the effects of 3.1 THz radiation on the expression of recombinant red fluorescent protein (RFP) in .

In recent years, many studies have been conducted to investigate the non-thermal effects of THz radiation on different organisms, but further studies are needed to fully elucidate the effects, especially on the molecular level. In this study, we explored the effects of at 3.1 THz radiation on protein expression in ) using red fluorescent protein as a reporter molecule.

Inhibition of PI3Kγ by AS605240 Protects tMCAO Mice by Attenuating Pro-Inflammatory Signaling and Cytokine Release in Reactive Astrocytes.

The intense and prolonged inflammatory response after ischemic stroke significantly contributes to the secondary neural injury. PI3Kγ, which is involved in the regulation of vascular permeability, chemotactic leukocyte migration and microglia activation, is a key target for intervention in the inflammatory response. In this study, we identified the protective effect of the PI3Kγ inhibitor AS605240 against stroke-related injury in the mouse model of transient intraluminal middle cerebral artery occlusion (tMCAO).

Beta-hydroxybutyrate Promotes the Expression of BDNF in Hippocampal Neurons under Adequate Glucose Supply.

Neurobiological evidence suggests that the ketone metabolite β-hydroxybutyrate (BHBA) exerts many neuroprotective functions for the brain. The previous study revealed that BHBA could promote the expression of brain-derived neurotrophic factor (BDNF) at glucose inadequate condition. Here we demonstrated that BHBA administration induced the expression of BDNF in the hippocampus of mice fed with normal diet.

Activated STING enhances Tregs infiltration in the HPV-related carcinogenesis of tongue squamous cells via the c-jun/CCL22 signal.

The negative role of the activated stimulator of IFN genes (STING) has been uncovered in autoinflammatory disease and cancer. However, the role of STING in virus-related carcinogenesis is not well known. Herein, HPV(+) tongue squamous cell carcinoma (TSCC) (n=25) and HPV(-) TSCC samples (n=25) were randomly collected and were verified by in situ hybridization (ISH) and p16 immunohistochemistry (IHC) to assess the expression and activated status of STING through IHC.

TLR9-induced miR-155 and Ets-1 decrease expression of CD1d on B cells in SLE.

B cells present lipid antigens to CD1d-restricted invariant natural killer T (iNKT) cells to maintain autoimmune tolerance, and this process is disrupted in systemic lupus erythematosus (SLE). Inflammation may inhibit CD1d expression to exacerbate the pathology of lupus. However, how inflammation regulates CD1d expression on B cells is unclear in SLE.

Serum IL-17F combined with VEGF as potential diagnostic biomarkers for oral squamous cell carcinoma.

Although interleukin (IL) 17A can promote angiogenesis in several tumors, there are limited clinical evidences on cancer about the correlation between serum vascular endothelial growth factor (VEGF) and IL-17F, which is the most homologous to IL-17A. In this study, serum concentration of IL-17F and VEGF from healthy (n = 28), leukoplakia (n = 15), and oral squamous cell carcinoma (OSCC) groups (n = 85) were assessed and showed that IL-17F level was remarkably downregulated from healthy group (394.3 pg/ml) to OSCC group (82.

Serum CCL2 and CCL3 as potential biomarkers for the diagnosis of oral squamous cell carcinoma.

Monocyte chemotactic protein-1 (MCP-1/CCL2) and macrophage inflammatory protein-1α (MIP-1α/CCL3) are small chemotactic proteins that have been found in several kinds of tumor tissue samples and function as key regulators of cancer progression. However, the expression of CCL2 and CCL3 in serum samples of oral squamous cell carcinoma (OSCC) patients remains unknown. This study aimed to investigate the prognostic meaning of serum CCL2 and CCL3 in OSCC.

A novel 1,2-benzenediamine derivative FC-99 suppresses TLR3 expression and ameliorates disease symptoms in a mouse model of sepsis.

Background And Purpose: Sepsis is a clinical condition characterized by overwhelming systemic inflammation with high mortality rate and high prevalence, but effective treatment is still lacking. Toll-like receptor 3 (TLR3) is an endogenous sensor, thought to regulate the amplification of immune response during sepsis. Modulators of TLR3 have an advantage in the treatment of sepsis.