Cited 0 times in

Involvement of the MAPK and PI3K pathways in chitinase 3-like 1-regulated hyperoxia-induced airway epithelial cell death

Title
 Involvement of the MAPK and PI3K pathways in chitinase 3-like 1-regulated hyperoxia-induced airway epithelial cell death
Authors
 Mi Na Kim; Kyung Eun Lee; Myung Hyun Sohn; Kyu Earn Kim; Kyung Won Kim; Won Il Heo; Jung Yeon Hong
Issue Date
2012
Journal Title
 Biochemical and Biophysical Research Communications
ISSN
 0006-291X
Citation
 Biochemical and Biophysical Research Communications, Vol.421(4) : 790~796, 2012
Abstract
BACKGROUND: Exposure to 100% oxygen causes hyperoxic acute lung injury characterized by cell death and injury of alveolar epithelial cells. Recently, the role of chitinase 3-like 1 (CHI3L1), a member of the glycosyl hydrolase 18 family that lacks chitinase activity, in oxidative stress was demonstrated in murine models. High levels of serum CHI3L1 have been associated with various diseases of the lung, such as asthma, chronic obstructive pulmonary disease, and cancer. However, the role of CHI3L1 in human airway epithelial cells undergoing oxidative stress remains unknown. In addition, the signaling pathways associated with CHI3L1 in this process are poorly understood. PURPOSE: In this study, we demonstrate the role of CHI3L1, along with the MAPK and PI3K signaling pathways, in hyperoxia-exposed airway epithelial cells. METHOD: The human airway epithelial cell line, BEAS-2B, was exposed to >95% oxygen (hyperoxia) for up to 72h. Hyperoxia-induced cell death was determined by assessing cell viability, Annexin-V FITC staining, caspase-3 and -7 expression, and electron microscopy. CHI3L1 knockdown and overexpression studies were conducted in BEAS-2B cells to examine the role of CHI3L1 in hyperoxia-induced apoptosis. Activation of the MAPK and PI3K pathways was also investigated to determine the role of these signaling cascades in this process. RESULTS: Hyperoxia exposure increased CHI3L1 expression and apoptosis in a time-dependent manner. CHI3L1 knockdown protected cells from hyperoxia-induced apoptosis. In contrast, CHI3L1 overexpression promoted cell death after hyperoxia exposure. Finally, phosphorylation of ERK1/2, p38, and Akt were affected by CHI3L1 knockdown. CONCLUSION: This study indicates that CHI3L1 is involved in hyperoxia-induced cell death, suggesting that CHI3L1 may be one of several cell death regulators influencing the MAPK and PI3K pathways during oxidative stress in human airway epithelial cells
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/89694
DOI
10.1016/j.bbrc.2012.04.085
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Pediatrics
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
Yonsei Authors
사서에게 알리기
  feedback
Link
 http://www.sciencedirect.com/science/article/pii/S0006291X12007528
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse