PMID- 14656700
OWN - NLM
STAT- MEDLINE
DCOM- 20040206
LR  - 20200930
IS  - 1040-0605 (Print)
IS  - 1040-0605 (Linking)
VI  - 286
IP  - 1
DP  - 2004 Jan
TI  - Expression and functional implications of CCR2 expression on murine alveolar 
      epithelial cells.
PG  - L68-72
AB  - Acute lung injury results in damage to the alveolar epithelium, leading to leak 
      of proteins into the alveolar space and impaired gas exchange. Lung function can 
      be restored only if the epithelial layer is restored. The process of 
      reepithelialization requires migration of lung epithelial cells to cover denuded 
      basement membranes. The factors that control the migration of lung epithelial 
      cells are incompletely understood. We examined isolated murine type II alveolar 
      epithelial cells (AECs) for expression of CC chemokine receptor 2 (CCR2) and 
      functional consequences of the binding of the main CCR2 ligand monocyte 
      chemoattractant protein-1 (MCP-1). We found that primary AECs bound MCP-1 and 
      expressed CCR2 mRNA. These cells demonstrated functional consequences of CCR2 
      expression with migration in response to MCP-1 in chemotaxis/haptotaxis assays. 
      Primary AECs cultured from mice lacking CCR2 did not respond to MCP-1. Monolayers 
      of AECs lacking CCR2 demonstrated delayed closure of mechanical wounds compared 
      with AEC monolayers expressing CCR2. Delayed closure of mechanical wounds of 
      wild-type AECs was also demonstrated in the presence of anti-MCP-1 antibody. 
      These data demonstrate for the first time that AECs express CCR2 and are capable 
      of using this receptor for chemotaxis and healing of wounds. CCR2-MCP-1 
      interactions may be important in the process of reepithelialization after lung 
      injury.
FAU - Christensen, Paul J
AU  - Christensen PJ
AD  - Division of Pulmonary and Critical Care Medicine, Departmentof Internal Medicine, 
      University of Michigan School of Medicine, and Pulmonary Section, Veterans 
      Affairs Medical Center, Ann Arbor, 48105, USA. pchriste@umich.edu
FAU - Du, Ming
AU  - Du M
FAU - Moore, Bethany
AU  - Moore B
FAU - Morris, Susan
AU  - Morris S
FAU - Toews, Galen B
AU  - Toews GB
FAU - Paine, Robert 3rd
AU  - Paine R 3rd
LA  - eng
GR  - 1P50 HL-56402/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol Lung Cell Mol Physiol
JT  - American journal of physiology. Lung cellular and molecular physiology
JID - 100901229
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - Cell Movement/drug effects/physiology
MH  - Chemokine CCL2/metabolism/pharmacology
MH  - Chemotaxis/drug effects/physiology
MH  - Gene Expression/physiology
MH  - In Vitro Techniques
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Pulmonary Alveoli/cytology/*physiology
MH  - RNA, Messenger/analysis
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/*genetics/*metabolism
MH  - Respiratory Mucosa/cytology/*physiology
MH  - Wound Healing/physiology
EDAT- 2003/12/06 05:00
MHDA- 2004/02/10 05:00
CRDT- 2003/12/06 05:00
PHST- 2003/12/06 05:00 [pubmed]
PHST- 2004/02/10 05:00 [medline]
PHST- 2003/12/06 05:00 [entrez]
AID - 286/1/L68 [pii]
AID - 10.1152/ajplung.00079.2003 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2004 Jan;286(1):L68-72. doi: 
      10.1152/ajplung.00079.2003.