Endothelial semaphorin 7A promotes seawater aspiration-induced acute lung injury through plexin C1 and β1 integrin.

Endothelial semaphorin 7A promotes seawater aspiration-induced acute lung injury through plexin C1 and β1 integrin.
Mol Med Rep. 2017 Jul 27;:
Authors: Zhang M, Yan X, Liu W, Sun R, Xie Y, Jin F
Abstract
Inflammation and edema are two main characteristics in seawater aspiration‑induced acute lung injury (ALI). In a previous study of the authors, it was demonstrated that endothelial semaphorin 7A (SEMA7A) serves an important role in the development of seawater‑induced inflammation and edema. However, the mechanism of endothelial SEMA7A‑mediated ALI remains unclear. Therefore, the authors explored the effect of SEMA7A in rat pulmonary microvascular endothelial cells (RPMVECs) and the interaction between endothelial SEMA7A and alveolar macrophages during seawater aspiration‑induced ALI. The role of SEMA7A in endothelial permeability was detected using plexin C1 blocking antibody or SEMA7A small interfering (si)RNA. In addition, RPMVECs were co‑cultured with rat alveolar macrophage cell line‑NR8383 cells and pro‑inflammatory cytokine production was detected. Interaction between the β1 integrin and SEMA7A was detected using the β1 integrin blocking antibody or SEMA7A siRNA. Seawater stimulation induced endothelial cytoskeleton remodeling, endothelial permeability, phosphorylation of cofilin, and increased the vascular endothelial growth factor (VEGF) expression in RPMVECs. Moreover, seawater stimulation led to expression ...

Source: Molecular Medicine Reports - August 4, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research