Search results for "FGF-2"
showing 3 items of 23 documents
Shed vesicles are involved in the release of some leaderless proteins.
2006
Most proteins destined for secretion in the extracellular matrix are characterized by the presence of N-terminal signal peptides which direct their translocation into the endoplasmic reticulum, they are subsequently transferred to the Golgi apparatus and then secreted in the extracellular space. A growing number of secreted proteins, are being identified which, however, lack signal peptides allowing their entrance into the endoplasmic reticulum. They include the inflammatory cytokine interleukin 1b, galactins, macrophage migration inhibitory factor (MIF), acid and basic fibroblast growth factors (FGF-1, FGF-2) and Sphingosine kinase1(SphK-1). These proteins are secreted from the cell by unc…
Angiogenic and/or pro-apoptotic factors are shed from brain cells via extracellular vesicles
2008
We set a three-cell type coculture system in which neurons and astrocytes synergistically induce brain capillary endothelial cells to form a monolayer with permeability properties resembling those of the physiological blood-brain barrier (BBB) (Schiera et al., 2003; Schiera et al., 2005). On the basis of immunofluorescence, scanner electron microscopy and western blot analyses, we also suggested that both astrocytes and neurons in culture shed extracellular vesicles that contain FGF-2 and VEGF, as well as beta1-integrin, a membrane protein that can be considered a marker of shedding (Schiera et al, 2007; Proia et al., 2008). In addition, it was already known that transformed glial cells (ol…
Nicotinic receptor agonists as neuroprotective/neurotrophic drugs. Progress in molecular mechanisms
2007
In the present work we reviewed recent advances concerning neuroprotective/neurotrophic effects of acute or chronic nicotine exposure, and the signalling pathways mediating these effects, including mechanisms implicated in nicotine addiction and nAChR desensitization. Experimental and clinical data largely indicate long-lasting effects of nicotine and nicotinic agonists that imply a neuroprotective/neurotrophic role of nAChR activation, involving mainly alpha 7 and alpha 4 beta 2 nAChR subtypes, as evidenced using selective nAChR agonists. Compounds interacting with neuronal nAChRs have the potential to be neuroprotective and treatment with nAChR agonists elicits long-lasting neurotrophic e…