TY - JOUR
T1 - Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)
AU - Lin, Jinfeng
AU - Sun, Zhaorui
AU - Zhang, Wei
AU - Liu, Hongmei
AU - Shao, Danbing
AU - Ren, Yi
AU - Wen, Yanfang
AU - Cao, Liping
AU - Wolfram, Joy
AU - Yang, Zhizhou
AU - Nie, Shinan
N1 - Funding Information:
This study was supported by a grant from the Major Projects Foundation of Nanjing Military Region (12Z32), the Medical Science Foundation for young cultivation project of PLA (13QNP038), and the Natural Science Foundation of Jinling Hospital (2013023 and 2014004).
Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2015/6/18
Y1 - 2015/6/18
N2 - The rapid repair of gastric mucosa is critical upon exposure to injurious agents. Intestinal trefoil factor (ITF) is a member of the trefoil factor family domain peptides, which play an important role in the cytoprotection of gastric epithelium. However, the underlying molecular mechanisms that are responsible for ITF-induced gastric epithelial repair remain unclear. In the present study, we demonstrate that ITF enhances the proliferation and migration of GES-1 gastric endothelial cells in a dose- and time-dependent manner through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the ITF-mediated protection of GES-1 cells from a NS398 (nonsteroidal anti-inflammatory drug) was dependent on the ERK1/2 signaling pathway. Taken together, the results provide a mechanistic explanation for ITF-mediated protection of gastric epithelial mucosa cells, suggesting that activation of the ERK1/2 signaling pathway may provide a new therapeutic strategy for repairing gastric injury.
AB - The rapid repair of gastric mucosa is critical upon exposure to injurious agents. Intestinal trefoil factor (ITF) is a member of the trefoil factor family domain peptides, which play an important role in the cytoprotection of gastric epithelium. However, the underlying molecular mechanisms that are responsible for ITF-induced gastric epithelial repair remain unclear. In the present study, we demonstrate that ITF enhances the proliferation and migration of GES-1 gastric endothelial cells in a dose- and time-dependent manner through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the ITF-mediated protection of GES-1 cells from a NS398 (nonsteroidal anti-inflammatory drug) was dependent on the ERK1/2 signaling pathway. Taken together, the results provide a mechanistic explanation for ITF-mediated protection of gastric epithelial mucosa cells, suggesting that activation of the ERK1/2 signaling pathway may provide a new therapeutic strategy for repairing gastric injury.
KW - Cytoprotection
KW - ERK1/2 signaling pathway
KW - Gastric mucosal epithelium
KW - Intestinal trefoil factor
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U2 - 10.1007/s11010-015-2386-2
DO - 10.1007/s11010-015-2386-2
M3 - Article
C2 - 25776570
AN - SCOPUS:84941740442
SN - 0300-8177
VL - 404
SP - 263
EP - 270
JO - Molecular and Cellular Biochemistry
JF - Molecular and Cellular Biochemistry
IS - 1-2
ER -