Lumican regulates ventilation-induced epithelial-mesenchymal transition through extracelluar signal-regulated kinase pathway.

ABSTRACT:

Background

Mechanical ventilation used in patients with acute lung injury can damage pulmonary epithelial cells through production of inflammatory cytokines and excess deposition of the extracellular matrix protein lumican. Lumican participates in macrophage inflammatory protein (MIP)-2 and transforming growth factor-β₁ (TGF-β₁) signaling during the fibroproliferative phase of acute lung injury, which involves a process of epithelial-mesenchymal transition (EMT). The mechanisms regulating interactions between mechanical ventilation and lung injury are unclear. We hypothesized that lung damage and EMT by high tidal volume (Vt) mechanical stretch causes upregulation of lumican that modulates MIP-2 and TGF-β₁ through the extracellular signal-regulated kinase (ERK) 1/2 pathway.

Meth

SUBMITTER: Li LF 

PROVIDER: S-EPMC3653345 | biostudies-literature | 2013 May

REPOSITORIES: biostudies-literature