A Promising Candidate: Heparin-Binding Protein Steps onto the Stage of Sepsis Prediction

Figure 2

HBP induces increased endothelial permeability that eventually results in vascular leakage. PMNs bind ECs to release HBP, and then HBP interacts with ECs through glycosaminoglycans. Once HBP is internalized via a receptor-mediated process, PKC and Rho kinase are activated, ultimately leading the rearrangement of the cytoskeleton and cell contraction. PKC also phosphorylates tight junction-related proteins to facilitate changes in the tight junctions between ECs. As a result, gaps form between ECs that ultimately result in vascular leakage.