Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells

Cha Xiang Guan; Yan Ru Cui; Guo Ying Sun; Fang Yu; Chun Yan Tang; Yun Chao Li; Hui Jun Liu; Xiang Fang

doi:10.1016/j.regpep.2008.12.003

Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells

Cha Xiang Guan, Yan Ru Cui, Guo Ying Sun, Fang Yu, Chun Yan Tang, Yun Chao Li, Hui Jun Liu, Xiang Fang

Neurology

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

20 Scopus citations

Abstract

Vasoactive intestinal peptide (VIP) is one of the most important sensory neuropeptides in respiratory system. We previously reported that VIP enhances wound healing and proliferation of human bronchial epithelial cells (HBECs), and these effects are mediated by intracellular signaling molecules such as protein kinase A (PKA), protein kinase C (PKC), Calmodulin (CaM), and extracellular signal-regulated kinase (ERK). In the present study, we further investigated the role of cAMP Response Element Binding Protein (CREB) in VIP-promoted protective effects in mechanical-damaged HBECs. VIP-mediated wound healing and cell proliferation in HBECs was inhibited by CREB antisense oligonucleotides (ASO) in a time-dependent manner. VIP increased the CREB DNA binding activity and expression of the p-CREB that were inhibited by VIP receptor antagonist. Increased CREB DNA binding activity and expression of the p-CREB were also partially inhibited by PKA and ERK inhibitors. These results suggest that the VIP-mediated wound repair of HBECs is associated with activation of CREB via PKA and ERK dependent pathway. Crown

Original language	English (US)
Pages (from-to)	64-69
Number of pages	6
Journal	Regulatory Peptides
Volume	153
Issue number	1-3
DOIs	https://doi.org/10.1016/j.regpep.2008.12.003
State	Published - Feb 25 2009

Keywords

DNA binding activity
Migration
Proliferation
Signal transduction
p-CREB

ASJC Scopus subject areas

Biochemistry
Physiology
Endocrinology
Clinical Biochemistry
Cellular and Molecular Neuroscience

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10.1016/j.regpep.2008.12.003

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title = "Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells",

abstract = "Vasoactive intestinal peptide (VIP) is one of the most important sensory neuropeptides in respiratory system. We previously reported that VIP enhances wound healing and proliferation of human bronchial epithelial cells (HBECs), and these effects are mediated by intracellular signaling molecules such as protein kinase A (PKA), protein kinase C (PKC), Calmodulin (CaM), and extracellular signal-regulated kinase (ERK). In the present study, we further investigated the role of cAMP Response Element Binding Protein (CREB) in VIP-promoted protective effects in mechanical-damaged HBECs. VIP-mediated wound healing and cell proliferation in HBECs was inhibited by CREB antisense oligonucleotides (ASO) in a time-dependent manner. VIP increased the CREB DNA binding activity and expression of the p-CREB that were inhibited by VIP receptor antagonist. Increased CREB DNA binding activity and expression of the p-CREB were also partially inhibited by PKA and ERK inhibitors. These results suggest that the VIP-mediated wound repair of HBECs is associated with activation of CREB via PKA and ERK dependent pathway. Crown",

keywords = "DNA binding activity, Migration, Proliferation, Signal transduction, p-CREB",

author = "Guan, {Cha Xiang} and Cui, {Yan Ru} and Sun, {Guo Ying} and Fang Yu and Tang, {Chun Yan} and Li, {Yun Chao} and Liu, {Hui Jun} and Xiang Fang",

note = "Funding Information: This work was supported in part by the National Natural Science Foundation of China (No. 30870915) and Hunan Provincial Natural Science Foundation of China (No. 07JJ3064). We thank Dr. Gruenert from the University of California, San Francisco, for providing an immortalized human BEC line 16HBE140-.",

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AU - Guan, Cha Xiang

AU - Cui, Yan Ru

AU - Sun, Guo Ying

AU - Yu, Fang

AU - Tang, Chun Yan

AU - Li, Yun Chao

AU - Liu, Hui Jun

AU - Fang, Xiang

N1 - Funding Information: This work was supported in part by the National Natural Science Foundation of China (No. 30870915) and Hunan Provincial Natural Science Foundation of China (No. 07JJ3064). We thank Dr. Gruenert from the University of California, San Francisco, for providing an immortalized human BEC line 16HBE140-.

PY - 2009/2/25

Y1 - 2009/2/25

N2 - Vasoactive intestinal peptide (VIP) is one of the most important sensory neuropeptides in respiratory system. We previously reported that VIP enhances wound healing and proliferation of human bronchial epithelial cells (HBECs), and these effects are mediated by intracellular signaling molecules such as protein kinase A (PKA), protein kinase C (PKC), Calmodulin (CaM), and extracellular signal-regulated kinase (ERK). In the present study, we further investigated the role of cAMP Response Element Binding Protein (CREB) in VIP-promoted protective effects in mechanical-damaged HBECs. VIP-mediated wound healing and cell proliferation in HBECs was inhibited by CREB antisense oligonucleotides (ASO) in a time-dependent manner. VIP increased the CREB DNA binding activity and expression of the p-CREB that were inhibited by VIP receptor antagonist. Increased CREB DNA binding activity and expression of the p-CREB were also partially inhibited by PKA and ERK inhibitors. These results suggest that the VIP-mediated wound repair of HBECs is associated with activation of CREB via PKA and ERK dependent pathway. Crown

AB - Vasoactive intestinal peptide (VIP) is one of the most important sensory neuropeptides in respiratory system. We previously reported that VIP enhances wound healing and proliferation of human bronchial epithelial cells (HBECs), and these effects are mediated by intracellular signaling molecules such as protein kinase A (PKA), protein kinase C (PKC), Calmodulin (CaM), and extracellular signal-regulated kinase (ERK). In the present study, we further investigated the role of cAMP Response Element Binding Protein (CREB) in VIP-promoted protective effects in mechanical-damaged HBECs. VIP-mediated wound healing and cell proliferation in HBECs was inhibited by CREB antisense oligonucleotides (ASO) in a time-dependent manner. VIP increased the CREB DNA binding activity and expression of the p-CREB that were inhibited by VIP receptor antagonist. Increased CREB DNA binding activity and expression of the p-CREB were also partially inhibited by PKA and ERK inhibitors. These results suggest that the VIP-mediated wound repair of HBECs is associated with activation of CREB via PKA and ERK dependent pathway. Crown

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KW - p-CREB

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Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells

Abstract

Keywords

ASJC Scopus subject areas

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