Moreover, our in vitro model revealed that VEGF mRNA and protein levels and VEGF receptors are increased by PMA or SIN-1 stimulation in chondrocytes and human articular cartilage explants.
Our data, although obtained in an in vitro model, revealed, for the first time, that high concentration of EVE may induce EMT in liver cells confirming previous published evidences obtained in renal cells.
Altogether, our data, although obtained by an in vitro model, reveal new biological/cellular aspects of the liver and systemic pro-fibrotic machinery induced by EVE treatment; if confirmed by additional studies, they could be useful for researchers to develop new therapeutic strategies that may prevent/minimize the systemic fibrotic adverse effects induced by high doses EVE therapy.
Altogether, our data, although obtained in an in vitro model, reveal new biological/cellular aspects of the liver and systemic pro-fibrotic machinery induced by high-dose EVE treatment; if confirmed by additional studies, they could be useful for researchers to develop new therapeutic strategies that may increase efficacy and reduce potential adverse affects of EVE also in the field of cancer.
Then, a series of in vitro co-culture models revealed that it was the secretion of soluble factors by chondrocytes but not cell cell contact that provided the chondrogenic signals.
In other diseases, in vitro models have revealed a number of key processes relevant to the clinical diseases [ 9, 12, 13] and it is likely that the responses identified here will prove to be equally important.
The in vitro wound model revealed an increasing wound healing rate with increasing doses of TTP treatment.
Proteomic analysis of three in vitro and two in vivo models revealed a decrease in antioxidant proteins that regulate H2O2 processing, by ≥2 fold in CF vs. matched normal controls.
The in vitro and in vivo TBI models revealed that RV treatment increased cell viability and reduced apoptosis and autophagy by suppressing ROS generation and GSK-3 β activation.
