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

Research output: Contribution to journalArticle

15 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)64-69
Number of pages6
JournalRegulatory Peptides
Volume153
Issue number1-3
DOIs
StatePublished - Feb 25 2009

Fingerprint

Cyclic AMP Response Element-Binding Protein
Vasoactive Intestinal Peptide
Wound Healing
Epithelial Cells
Extracellular Signal-Regulated MAP Kinases
Cyclic AMP-Dependent Protein Kinases
Protein Binding
Vasoactive Intestinal Peptide Receptors
Respiratory system
Antisense Oligonucleotides
DNA
Cell proliferation
Calmodulin
Neuropeptides
Crowns
Respiratory System
Protein Kinase C
Repair
Chemical activation
Cell Proliferation

Keywords

  • DNA binding activity
  • Migration
  • p-CREB
  • Proliferation
  • Signal transduction

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Endocrinology
  • Physiology
  • Cellular and Molecular Neuroscience

Cite this

Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells. / Guan, Cha Xiang; Cui, Yan Ru; Sun, Guo Ying; Yu, Fang; Tang, Chun Yan; Li, Yun Chao; Liu, Hui Jun; Fang, Xiang.

In: Regulatory Peptides, Vol. 153, No. 1-3, 25.02.2009, p. 64-69.

Research output: Contribution to journalArticle

Guan, Cha Xiang ; Cui, Yan Ru ; Sun, Guo Ying ; Yu, Fang ; Tang, Chun Yan ; Li, Yun Chao ; Liu, Hui Jun ; Fang, Xiang. / Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells. In: Regulatory Peptides. 2009 ; Vol. 153, No. 1-3. pp. 64-69.
@article{7fdabfb5e15d4e96b41c8226e5d2f8e0,
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, p-CREB, Proliferation, Signal transduction",
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",
year = "2009",
month = "2",
day = "25",
doi = "10.1016/j.regpep.2008.12.003",
language = "English (US)",
volume = "153",
pages = "64--69",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - Role of CREB in vasoactive intestinal peptide-mediated wound healing in human bronchial epithelial cells

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

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

KW - DNA binding activity

KW - Migration

KW - p-CREB

KW - Proliferation

KW - Signal transduction

UR - http://www.scopus.com/inward/record.url?scp=59849123359&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=59849123359&partnerID=8YFLogxK

U2 - 10.1016/j.regpep.2008.12.003

DO - 10.1016/j.regpep.2008.12.003

M3 - Article

VL - 153

SP - 64

EP - 69

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

IS - 1-3

ER -