PMID- 9709377
OWN - NLM
STAT- MEDLINE
DCOM- 19981023
LR  - 20190512
IS  - 0959-9673 (Print)
IS  - 1365-2613 (Electronic)
IS  - 0959-9673 (Linking)
VI  - 79
IP  - 2
DP  - 1998 Apr
TI  - Morphological alteration of cultured tracheobronchial epithelial cells is 
      accompanied by the expression of chemokines, MCP-1 and CINC/gro, in rats.
PG  - 81-92
AB  - Morphologically altered epithelial cells are generally observed in fibrotic lung 
      conditions and have been reported to produce several cytokines. To examine the 
      relationship between morphological changes of the tracheobronchial epithelial 
      cells (TBECs) and their chemokine production, we investigated, (1) the mRNA 
      expression and protein secretion of monocyte chemoattractant protein-1 (MCP-1) 
      and cytokine-induced neutrophil chemoattractant/gro (CINC/gro), (2) morphological 
      changes by electron microscopy, and (3) cytokeratin (CK) expression, using a 
      primary culture system of rat TBECs. The constitutive secretion of MCP-1 in the 
      culture supernatant of TBECs increased in a time-dependent manner, whereas the 
      CINC/gro secretion was not changed. These results were consistent with the 
      chemokines' mRNA expression observed by in situ hybridization. The constitutive 
      secretions of MCP-1 and CINC/gro were inhibited partially but significantly by 
      dexamethasone. With the extension of the culture period, the morphology of the 
      TBECs became flat and spindle in shape, similar to squamous metaplasia, as 
      observed on electron microscopy, and with strong expression of CK 14. Sequential 
      staining using immunocytochemistry and in situ hybridization revealed the 
      coexpression of MCP-1 mRNA and CK 14. These data indicate a significant 
      relationship between the morphological squamoid alteration and the constitutive 
      expression of MCP-1 but not of CINC/gro. It is thought that the squamous 
      metaplasia of TBECs may accompany the alteration of cytokine production and play 
      an important role in chronic lung inflammation.
FAU - Yamamoto, T
AU  - Yamamoto T
AD  - First Department of Internal Medicine, Kumamoto University School of Medicine, 
      Japan.
FAU - Iyonaga, K
AU  - Iyonaga K
FAU - Takeya, M
AU  - Takeya M
FAU - Saita, N
AU  - Saita N
FAU - Suga, M
AU  - Suga M
FAU - Ando, M
AU  - Ando M
FAU - Takahashi, K
AU  - Takahashi K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Int J Exp Pathol
JT  - International journal of experimental pathology
JID - 9014042
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cxcl1 protein, rat)
RN  - 0 (Growth Substances)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 68238-35-7 (Keratins)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Animals
MH  - Bronchi/drug effects/*metabolism/*ultrastructure
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - Chemokine CXCL1
MH  - *Chemokines, CXC
MH  - Chemotactic Factors/*metabolism
MH  - Dexamethasone/pharmacology
MH  - Epithelium/drug effects/metabolism
MH  - Growth Substances/*metabolism
MH  - Immunoenzyme Techniques
MH  - In Situ Hybridization
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Interleukin-1/pharmacology
MH  - Keratins/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Microscopy, Electron
MH  - Microscopy, Phase-Contrast
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Trachea/drug effects/*metabolism/*ultrastructure
PMC - PMC3230834
EDAT- 1998/08/26 00:00
MHDA- 1998/08/26 00:01
PMCR- 1999/04/01
CRDT- 1998/08/26 00:00
PHST- 1998/08/26 00:00 [pubmed]
PHST- 1998/08/26 00:01 [medline]
PHST- 1998/08/26 00:00 [entrez]
PHST- 1999/04/01 00:00 [pmc-release]
AID - 10.1046/j.1365-2613.1998.00043.x [doi]
PST - ppublish
SO  - Int J Exp Pathol. 1998 Apr;79(2):81-92. doi: 10.1046/j.1365-2613.1998.00043.x.