PMID- 7525714
OWN - NLM
STAT- MEDLINE
DCOM- 19941207
LR  - 20071114
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 153
IP  - 10
DP  - 1994 Nov 15
TI  - Lung monocyte chemoattractant protein-1 gene expression in bleomycin-induced 
      pulmonary fibrosis.
PG  - 4733-41
AB  - Recent studies indicate that monocyte chemoattractant protein-1 (MCP-1) may play 
      an important role in pulmonary inflammation. In vitro studies show that a number 
      of cell types are capable of producing MCP-1. In this study, MCP-1 expression in 
      lungs of rats with bleomycin (BLM)-induced pulmonary fibrosis is examined to 
      evaluate its cellular origin and potential role in pathogenesis. Lung fibrosis 
      was induced in male Fisher 344 rats by endotracheal injection on day 0. On 
      selected days after injection, lungs were harvested for in situ and Northern 
      hybridization analyses for MCP-1 mRNA expression, immunochemical and 
      histochemical analyses for MCP-1 protein expression, and identification of cell 
      type. Northern analysis revealed significant elevation in lung MCP-1 mRNA 
      expression beginning on day 3 post-BLM treatment, increasing to a peak on day 7, 
      and then decreasing toward control levels after day 21. In situ hybridization 
      combined with histochemical staining with chromotrope 2R indicate that most of 
      the cells expressing MCP-1 mRNA at these time points are primarily eosinophils. A 
      few scattered reactive fibroblasts, some mononuclear cells, epithelial cells, and 
      cells of certain blood vessel walls also express this mRNA. Increased MCP-1 
      protein expression also was found to be predominantly within and adjacent to 
      eosinophils. The eosinophils expressing this mRNA were found predominantly within 
      areas of active fibrosis. The kinetics of increase in the number of cells 
      expressing significant MCP-1 mRNA in lung sections paralleled that for MCP-1 mRNA 
      expression, as assessed by Northern analysis. These results, for the first time, 
      demonstrate that MCP-1 is up-regulated significantly in this rat animal model, 
      and that infiltrating eosinophils represent the major cellular source for this 
      increased MCP-1 expression.
FAU - Zhang, K
AU  - Zhang K
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.
FAU - Gharaee-Kermani, M
AU  - Gharaee-Kermani M
FAU - Jones, M L
AU  - Jones ML
FAU - Warren, J S
AU  - Warren JS
FAU - Phan, S H
AU  - Phan SH
LA  - eng
GR  - HL28737/HL/NHLBI NIH HHS/United States
GR  - HL31963/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 11056-06-7 (Bleomycin)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Bleomycin
MH  - Blotting, Northern
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis
MH  - Cytokines/*biosynthesis
MH  - Gene Expression Regulation/genetics
MH  - Immunoenzyme Techniques
MH  - In Situ Hybridization
MH  - Lung/*immunology/pathology
MH  - Male
MH  - Molecular Sequence Data
MH  - Pulmonary Fibrosis/chemically induced/*immunology/pathology
MH  - Rats
MH  - Rats, Inbred F344
EDAT- 1994/11/15 00:00
MHDA- 1994/11/15 00:01
CRDT- 1994/11/15 00:00
PHST- 1994/11/15 00:00 [pubmed]
PHST- 1994/11/15 00:01 [medline]
PHST- 1994/11/15 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1994 Nov 15;153(10):4733-41.