Role of adipocytokines in endometrial cancer progression.

Endometrial cancer is considered a significant barrier to increasing life expectancy and remains one of the most common malignant cancers among women in many countries worldwide. The increasing mortality rates are potentially proportional to the increasing obesity incidence. Adipose tissue secretes numerous adipocytokines, which may play important roles in endometrial cancer progression.

Chronic allergic asthma alters m6A epitranscriptomic tagging of mRNAs and lncRNAs in the lung.

To evaluate the role of m6A methylation of mRNAs and long non-coding RNAs (lncRNAs) in chronic allergic asthma. Transcriptome-wide N6-methyladenosine (m6A) changes in BALB/c mice were profiled using immunoprecipitated methylated RNAs with microarrays in lung with chronic allergic asthma. Gene ontology (GO) and KEGG analyses were conducted.

P2X7 receptor-mediated phenotype switching of pulmonary artery smooth muscle cells in hypoxia.

P2X7R activation contributes to the pathogenesis of pulmonary hypertension. However, the molecular mechanism through which P2X7R participates in pulmonary vascular remodeling is largely unknown. The rats and pulmonary artery smooth muscle cells (PASMCs) were maintained under hypoxia.

P2X4R promotes airway remodeling by acting on the phenotype switching of bronchial smooth muscle cells in rats.

The P2X4 receptor (P2X4R) contributes to airway inflammation and airway remodeling in mice with allergic asthma. However, the molecular mechanism by which P2X4R affects the airway remodeling in allergic asthma remains largely unknown. We established an allergic asthma model by ovalbumin (OVA) inhalation in BALB/c mice.

5-BDBD ameliorates an OVA-induced allergic asthma by the reduction of Th2 cytokines production.

Objectives: P2X4R is expressed in immunocyte and lung tissues. It has been a focus in inflammatory responses recently. This study investigated whether blockage of P2X4R attenuates allergic inflammation by modulating T cell response in ovalbumin-sensitized mice.

Hypoxia decrease expression of cartilage oligomeric matrix protein to promote phenotype switching of pulmonary arterial smooth muscle cells.

Extracellular matrix proteins play important roles in the development of pulmonary hypertension(pH). However, the role of Cartilage oligomeric matrix protein (COMP) in the development of hypoxia-induced pH is largely unknown. We tested the hypothesis that COMP deficiency induced by hypoxia leads to the phenotype switching of pulmonary arterial smooth muscle cells (PASMCs).

Tissue transglutaminase-1 promotes stemness and chemoresistance in gastric cancer cells by regulating Wnt/β-catenin signaling.

Gastric cancer is a common malignancy, and is one of the most frequent causes of cancer deaths worldwide. Recently, members of the transglutaminases (TGM) family, especially TGM2, have been implicated in the progression and drug resistance of cancers, but the function of TGM1 in cancer development has been largely overlooked. In this study, we demonstrate the roles of TGM1 in development of gastric cancer.

Effect of P2X4R on airway inflammation and airway remodeling in allergic airway challenge in mice.

P2X4 receptor (P2X4R) is the most widely expressed subtype of the P2XRs in the purinergic receptor family. Adenosine triphosphate (ATP), a ligand for this receptor, has been implicated in the pathogenesis of asthma. ATP‑P2X4R signaling is involved in pulmonary vascular remodeling, and in the proliferation and differentiation of airway and alveolar epithelial cell lines.

Interaction of integrin β4 with S1P receptors in S1P- and HGF-induced endothelial barrier enhancement.

We previously reported sphingosine 1-phosphate (S1P) and hepatocyte growth factor (HGF) augment endothelial cell (EC) barrier function and attenuate murine acute lung inury (ALI). While the mechanisms underlying these effects are not fully understood, S1P and HGF both transactivate the S1P receptor, S1PR1 and integrin β4 (ITGB4) at membrane caveolin-enriched microdomains (CEMs). In the current study, we investigated the roles of S1PR2 and S1PR3 in S1P/HGF-mediated EC signaling and their associations with ITGB4.

Enhancement of the nonamyloidogenic pathway by exogenous NGF in an Alzheimer transgenic mouse model.

Nerve growth factor (NGF) is an important nerve cell growth regulatory factor and has an indispensable role in the development, survival and regeneration of the cholinergic basal forebrain (CBF) neurons, and it has multiple targets when used for Alzheimer's Disease (AD) therapy. In this study, we observed whether NGF can affect cholinergic neurons to change amyloid-β precursor protein (APP) metabolism process and reduce amyloidosis in AD brains. NGF was administered intranasally to APP/PS1 double-transgenic mice for 14weeks.

Blockade of ankyrin repeat-rich membrane spanning protein modulates extracellular signal-regulated kinase expression and inhibits allergic inflammation in ovalbumin-sensitized mice.

Ankyrin repeat-rich membrane spanning protein (ARMS), also known as kinase D-interacting substrate of 220 kDa (Kidins220), is a transmembrane protein that has been reported to be involved in the pathogenesis of asthma through the nerve growth factor (NGF)/tyrosine kinase A (TrkA) receptor signaling pathway. To investigate whether NGF/TrkA-Kidins220/ARMS-extracellular signal-regulated kinase (ERK) signaling is activated in airway inflammation of asthma, BALB/c mice were sensitized and challenged with ovalbumin (OVA). The effects of Kidins220/ARMS on ERK, interleukin (IL)-1β, IL-4 and tumor necrosis factor (TNF)-α in lung tissues following the allergic airway challenge in mice were assessed by administering anti-ARMS antibody to the mice.

Expression of neuronal protein Kidins220/ARMS in the spleen and peripheral blood of mice following airway allergen challenge.

Nerve growth factor (NGF), combined with the high-affinity tyrosine kinase receptor A (TrkA), has been reported to be involved in the pathogenesis of asthma. Ankyrin-rich membrane spanning/transmembrane substrate of protein kinase D (ARMS/Kidins220), a TrkA‑binding protein, modulates the NGF signaling pathway. The aim of the present study was to investigate the expression of Kidins220/ARMS and the effect NGF has on the protein in the spleen and peripheral blood, following airway allergen challenge in mice.

Pharmacogenomics discovery and implementation in genome-wide association studies era.

Clinical response to therapeutic treatments often varies among individual patients, ranging from beneficial effect to even fatal adverse reaction. Pharmacogenomics holds the promise of personalized medicine through elucidating genetic determinants responsible for pharmacological outcomes (e.g.

NGF/TrkA-mediated Kidins220/ARMS signaling activated in the allergic airway challenge in mice.

Background: Nerve growth factor (NGF), combined with its high-affinity receptor tyrosine kinase receptor A (TrkA), has been reported to be involved in the pathogenesis of asthma.

Objective: To investigate whether the downstream protein ankyrin-rich membrane spanning (ARMS), a novel transmembrane substrate of protein kinase D (Kidins220), is activated in the pathogenesis of asthma.

Methods: The asthmatic model was established by the inhalation of ovalbumin in BALB/c mice.

Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice.

BALB/c mice were sensitized and challenged with ovalbumin. We hypothesized that Kidins220/ARMS influences airway inflammation and hyper-responsiveness during allergic airway challenge, and assessed it by intranasal administration of anti-NGF antibody or anti-ARMS antibody to mice. Airway resistance was measured using a sealed whole-body plethysmograph.