Involvement of Endoplasmic Reticulum Stress in Myofibroblastic Differentiation of Lung Fibroblasts

• DOI: 10.1165/rcmb.2011-0121oc
• Publication Date: 2011-08-19T03:47:33Z
• Authors: Hyun Ah Baek; Do Sung Kim; Ho Sung Park; Kyu Yun Jang; Myoung Jae Kang; Dong Geun Lee; Woo Sung Moon; Han Jung Chae; Myoung Ja Chung
• Keywords: Reticulum

Stress that impairs endoplasmic reticulum (ER) function leads to an accumulation of unfolded or misfolded proteins in the ER (ER stress) and triggers protein response (UPR). Recent studies suggest stress is involved idiopathic pulmonary fibrosis (IPF). The present study was undertaken determine role on myofibroblastic differentiation fibroblasts. Fibroblasts fibroblastic foci IPF showed immunoreactivity for GRP78. To α-smooth muscle actin (α-SMA) collagen type I expression fibroblasts, mouse human lung fibroblasts were treated with TGF-β1, stress-related proteins, α-SMA, analyzed by Western blotting. TGF-β1 significantly increased GRP78, XBP-1, ATF6α, which accompanied increases α-SMA A chemical chaperone, 4-PBA, suppressed TGF-β1-induced UPR induction. We also mediated through reactive oxygen species generation. Our provides first evidence implicating during fibrosis. These findings chaperones may improve our understanding pathogenesis IPF.