Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)

Jinfeng Lin; Zhaorui Sun; Wei Zhang; Hongmei Liu; Danbing Shao; Yi Ren; Yanfang Wen; Liping Cao; Joy Wolfram; Zhizhou Yang; Shinan Nie

doi:10.1007/s11010-015-2386-2

Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)

Jinfeng Lin, Zhaorui Sun, Wei Zhang, Hongmei Liu, Danbing Shao, Yi Ren, Yanfang Wen, Liping Cao, Joy Wolfram, Zhizhou Yang, Shinan Nie

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	263-70
Number of pages	8
Journal	Molecular and Cellular Biochemistry
Volume	404
Issue number	1-2
DOIs	https://doi.org/10.1007/s11010-015-2386-2
State	Published - Jun 2015

Keywords

Cell Line
Cell Movement
Cell Proliferation
Epithelium
Gastric Mucosa
Humans
MAP Kinase Signaling System
Nitrobenzenes
Peptides
Sulfonamides
Trefoil Factor-2
Journal Article
Research Support, Non-U.S. Gov't

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10.1007/s11010-015-2386-2

Cite this

Lin, J., Sun, Z., Zhang, W., Liu, H., Shao, D., Ren, Y., Wen, Y., Cao, L., Wolfram, J., Yang, Z., & Nie, S. (2015). Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Molecular and Cellular Biochemistry, 404(1-2), 263-70. https://doi.org/10.1007/s11010-015-2386-2

Lin, J, Sun, Z, Zhang, W, Liu, H, Shao, D, Ren, Y, Wen, Y, Cao, L, Wolfram, J, Yang, Z & Nie, S 2015, 'Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)', Molecular and Cellular Biochemistry, vol. 404, no. 1-2, pp. 263-70. https://doi.org/10.1007/s11010-015-2386-2

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title = "Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)",

abstract = "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.",

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author = "Jinfeng Lin and Zhaorui Sun and Wei Zhang and Hongmei Liu and Danbing Shao and Yi Ren and Yanfang Wen and Liping Cao and Joy Wolfram and Zhizhou Yang and Shinan Nie",

year = "2015",

month = jun,

doi = "10.1007/s11010-015-2386-2",

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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

PY - 2015/6

Y1 - 2015/6

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 - Cell Line

KW - Cell Movement

KW - Cell Proliferation

KW - Epithelium

KW - Gastric Mucosa

KW - Humans

KW - MAP Kinase Signaling System

KW - Nitrobenzenes

KW - Peptides

KW - Sulfonamides

KW - Trefoil Factor-2

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

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DO - 10.1007/s11010-015-2386-2

M3 - Article

C2 - 25776570

SN - 0300-8177

VL - 404

SP - 263

EP - 270

JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

IS - 1-2

ER -

Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)

Abstract

Keywords

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