Leukocyte transendothelial migration
Core of basic research: It clarifies the multi-step molecular mechanism by which leukocytes (neutrophils, monocytes, lymphocytes) cross the endothelial cell layer from the bloodstream into inflammatory tissues, including three key stages: "rolling-adhesion-migration". First, leukocytes bind to ligands on the endothelial cell surface via the Selectin family (L-Selectin, E-Selectin) to produce rolling; subsequently, Integrins (αLβ2, α4β1) on the leukocyte surface are activated and bind to ICAM-1 and VCAM-1 on endothelial cells to achieve stable adhesion; finally, leukocytes cross the endothelial cell junctions via PECAM-1-mediated homotypic interactions (dependent on Rho GTPase-regulated cytoskeletal rearrangement). Research focuses include the signal mechanism of Integrin activation, dynamic regulation of endothelial cell junctions, migration differences between different leukocyte subtypes, and abnormal enhancement of migration in inflammatory diseases (e.g., arthritis, asthma).
Core key proteins: Adhesion molecules (ICAM-1, VCAM-1, Selectin family), Integrin (αLβ2, α4β1, α4β7), PECAM-1 (platelet-endothelial cell adhesion molecule), Rho GTPases (Rac1, RhoA), PI3K, Akt, MAPK, VE-cadherin (endothelial cell junction molecule), CXCL8 (chemokine, activates Integrin).
Core key proteins: Adhesion molecules (ICAM-1, VCAM-1, Selectin family), Integrin (αLβ2, α4β1, α4β7), PECAM-1 (platelet-endothelial cell adhesion molecule), Rho GTPases (Rac1, RhoA), PI3K, Akt, MAPK, VE-cadherin (endothelial cell junction molecule), CXCL8 (chemokine, activates Integrin).
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