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Hepatogenic differentiation of human mesenchymal stem cells from adipose tissue in comparison with bone marrow mesenchymal stem cells.
ADSCs have a similar hepatogenic differentiation potential to BMSC, but a longer culture period and higher proliferation capacity, and may become an alternative for hepatocyte regeneration, liver cell transplantation or preclinical drug testing. Expand
Redox signaling in the gastrointestinal tract.
Redox signaling plays a critical role in the physiology and pathophysiology of gastrointestinal tract and in colorectal cancer, and exhibits two Janus faces: on the one hand, NOX1 up-regulation and derived hydrogen peroxide enhance Wnt/β-catenin and Notch proliferating pathways; on the other hand, ROS may disrupt tumor progression through different pro-apoptotic mechanisms. Expand
Neural differentiation from human embryonic stem cells as a tool to study early brain development and the neuroteratogenic effects of ethanol.
It is demonstrated that ethanol exposure impairs NPs survival, affects the differentiation of NPs into neurons and astrocytes, disrupts the actin cytoskeleton, and affects the expression of different genes associated with neural differentiation. Expand
Human mesenchymal stem cells from adipose tissue: Differentiation into hepatic lineage.
The results indicate that, under certain specific inducing conditions, ADSCs can be induced to differentiate into hepatic lineage in vitro, and may be an ideal source of high amounts of autologous stem cells. Expand
p38 MAPK: A dual role in hepatocyte proliferation through reactive oxygen species
P38α influences the redox balance, determining cell survival, terminal differentiation, proliferation, and senescence, and cells that have developed mechanisms to uncouple p38 MAPK activation from oxidative stress are more likely to become tumorigenic. Expand
Liver‐specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice
A key role is highlighted in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis and in survival during chronic inflammation such as biliary hepatitis. Expand
RhoE stimulates neurite‐like outgrowth in PC12 cells through inhibition of the RhoA/ROCK‐I signalling
J. Neurochem. (2010) 112, 1074–1087.
Targeted delivery of Cyclosporine A by polymeric nanocarriers improves the therapy of inflammatory bowel disease in a relevant mouse model
This study corroborates the potential of nanocarriers enabling an improved topical delivery of CYA to the inflamed gut mucosa after oral administration yielding the same improvement of disease parameters at only half the dose in comparison to microparticles and a commercial oral formulation, respectively, and at the same time minimizing systemic exposure and associated adverse effect. Expand
RhoE participates in the stimulation of the inflammatory response induced by ethanol in astrocytes.
The findings suggest that this small GTPase is involved in the stimulation of the inflammatory signaling induced by ethanol in astrocytes, and provides new insights into the molecular mechanism involved with the inflammatory responses in astroglial cells. Expand
Left ventricular cavity area reflects N-terminal pro-brain natriuretic peptide plasma levels in heart failure.
It is shown that when adjusted for age and BMI, LVFAC and LVESAI are independent predictors of NT-proBNP levels in both dilated and ischemic etiologies, and think LV areas are a useful and reproducible parameter, do not need geometric assumptions and reflect NT- ProBNP plasma levels. Expand