Proteases and small intestinal barrier function in health and disease.
London, United Kingdom. In Curr Opin Gastroenterol, Mar 2014
RECENT FINDINGS: It is now well established that intestinal proteases, such as matrix metalloproteinase (MMP)-1, MMP-3, MMP-10 and MMP-12, are key players in the development of ulcers in inflammatory bowel disease, have direct effects on epithelial barrier function and are involved in epithelial restitution.
Hemorrhagic transformation after ischemic stroke in animals and humans.
Sacramento, United States. In J Cereb Blood Flow Metab, Feb 2014
This contrasts to delayed HT (>18 to 24 hours after stroke) that relates to ischemia activation of brain proteases (MMP-2, MMP-3, MMP-9, and endogenous tissue plasminogen activator), neuroinflammation, and factors that promote vascular remodeling (vascular endothelial growth factor and high-moblity-group-box-1). Processes that mediate BBB repair and reduce HT risk are discussed, including transforming growth factor beta signaling in monocytes, Src kinase signaling, MMP inhibitors, and inhibitors of reactive oxygen species.
Biomarkers in vasculitis.
Boston, United States. In Curr Opin Rheumatol, Jan 2014
More conventional hypothesis-based studies have indicated that the following circulating proteins have potential to improve upon clinically available tests: pentraxin-3 in giant cell arteritis and Takayasu's arteritis; von Willebrand factor antigen in childhood central nervous system vasculitis; eotaxin-3 and other markers related to eosinophils or Th2 immune responses in eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome); and matrix metalloproteinase-3, tissue inhibitor of metalloproteinase-1, and CXCL13 in ANCA-associated vasculitis.
P2X7 Mediates ATP-Driven Invasiveness in Prostate Cancer Cells.
Beijing, China. In Plos One, Dec 2013
In addition, silencing of P2X7 remarkably attenuated ATP- or BzATP- driven expression changes of EMT/invasion-related genes Snail, E-cadherin, Claudin-1, IL-8 and MMP-3, and weakened the phosphorylation of PI3K/AKT and ERK1/2 in vitro.
Exercise, GLUT4, and skeletal muscle glucose uptake.
Copenhagen, Denmark. In Physiol Rev, Jul 2013
AMPK and CaMKII are key signaling kinases that appear to regulate GLUT4 expression via the HDAC4/5-MEF2 axis and MEF2-GEF interactions resulting in nuclear export of HDAC4/5 in turn leading to histone hyperacetylation on the GLUT4 promoter and increased GLUT4 transcription.