| Literature DB >> 26374984 |
Ryan T Jones1, Luis H Toledo-Pereyra2, Kelly M Quesnelle3.
Abstract
Liver ischemia reperfusion injury is mediated by a complex system of signaling cascades and inflammatory response resulting in organ damage. Selectins are a group of cell adhesion glycoproteins that play a key role in the initial immunological response. L-selectins, found on leukocytes, initiate the original adhesion and rolling phase of leukocyte extravasation upon liver sinusoidal endothelial cells (LSECs). P-selectins, found on platelets and tissue-specific endothelial cells, further increases leukocyte-endothelial adhesion and rolling. P-selectin-ligand binding also initiates intracellular signals that produce adhesion molecules to start firm adhesion and increase local chemokine production. L-selectin-ligand binding on the leukocytes increases adhesion molecule expression and chemokines, but also initiate changes in intracellular structural actin. E-selectin expression occurs with the presence of TNF-α and/or IL-1β. E-selectin-ligand binding decreases leukocyte rolling velocity and increases adhesion molecules. Together, these glycoproteins transition the leukocyte response from original margination and rolling to firm adhesion and eventually migration.Entities:
Keywords: IR; e-selectin; ischemia reperfusion; l-selectin; liver; p-selectin; selectins
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Year: 2015 PMID: 26374984 DOI: 10.3109/08941939.2015.1056920
Source DB: PubMed Journal: J Invest Surg ISSN: 0894-1939 Impact factor: 2.533