Intestinal dual-specificity phosphatase 6 regulates the cold-induced gut microbiota remodeling to promote white adipose browning.

Gut microbiota rearrangement induced by cold temperature is crucial for browning in murine white adipose tissue. This study provides evidence that DUSP6, a host factor, plays a critical role in regulating cold-induced gut microbiota rearrangement. When exposed to cold, the downregulation of intestinal DUSP6 increased the capacity of gut microbiota to produce ursodeoxycholic acid (UDCA).

Identification of a gut microbiota member that ameliorates DSS-induced colitis in intestinal barrier enhanced Dusp6-deficient mice.

Strengthening the gut epithelial barrier is a potential strategy for management of gut microbiota-associated illnesses. Here, we demonstrate that dual-specificity phosphatase 6 (Dusp6) knockout enhances baseline colon barrier integrity and ameliorates dextran sulfate sodium (DSS)-induced colonic injury. DUSP6 mutation in Caco-2 cells enhances the epithelial feature and increases mitochondrial oxygen consumption, accompanied by altered glucose metabolism and decreased glycolysis.

Proteomic and microbial assessments on the effect of Antrodia cinnamomea in C57BL/6 mice.

Antrodia cinnamomea (AC) is a nutraceutical fungus and studies have suggested that AC has the potential to prevent or alleviate diseases. However, little is known about the AC-induced phenotypes on the intestine-liver axis and gut microbial alterations. Here, we performed two-dimensional difference gel electrophoresis (2D-DIGE) and MALDI-Biotyper to elaborate the AC-induced phenotypes on the intestine-liver axis and gut microbial distribution of C57BL/6 mice.

Confers Obesity Resistance and Restores Intestinal Barrier Integrity in Leptin-deficient Obese Mice.

Obesity is associated with metabolic disorders. Thus, obesity prevention and treatment are essential for health. (AC) is a multifunctional medicinal fungus used for the treatment of various diseases and for preventing diet-induced obesity.

Wild-type p53 upregulates an early onset breast cancer-associated gene GAS7 to suppress metastasis via GAS7-CYFIP1-mediated signaling pathway.

The early onset breast cancer patients (age ≤ 40) often display higher incidence of axillary lymph node metastasis, and poorer five-year survival than the late-onset patients. To identify the genes and molecules associated with poor prognosis of early onset breast cancer, we examined gene expression profiles from paired breast normal/tumor tissues, and coupled with Gene Ontology and public data base analysis. Our data showed that the expression of GAS7b gene was lower in the early onset breast cancer patients as compared to the elder patients.

Strain-specific BDNF expression of rat primary astrocytes.

By producing brain-derived neurotrophic factor (BDNF), astrocytes play a role in disease resistance. This study was undertaken to investigate whether primary astrocytes derived from LEW/N and F344/N rats differentially express BDNF. LEW/N astrocytes expressed more BDNF mRNA and protein than F344/N astrocytes in basal and valproic acid (VPA)-stimulated conditions.

Strain-dependent inflammatory responsiveness of rat microglial cells.

The aim of this study is to test whether inflammatory responsiveness of rat microglial cells is strain-specific in primary microglia derived from neonatal LEW/N and F344/N rats. In contrast to F344/N microglia, LEW/N microglia constitutively and upon lipopolysaccharide challenge expressed higher levels of mRNA for the majority of inflammatory mediators studied. In addition, LEW/N microglia exhibited enhanced secretion of tumor necrosis factor-alpha and CCL2, as well as elevated nitric oxide production.

Cholesterol deficiency increases the vulnerability of hippocampal glia in primary culture to glutamate-induced excitotoxicity.

Cholesterol, a molecule critical for cellular function, is found in particular high concentration in the brain and has been implicated to synaptic plasticity and neuronal regeneration. This study was undertaken to investigate the mechanism by which cholesterol shortage modulates glutamate (Glu)-induced excitotoxicity in hippocampal cell cultures. A combined treatment of lovastatin and beta-cyclodextrin reduced cellular content of cholesterol while having no significant effect on cell viability in neuron/glia mixed cultures.