PMID- 11768716
OWN - NLM
STAT- MEDLINE
DCOM- 20020502
LR  - 20191025
IS  - 0190-2148 (Print)
IS  - 0190-2148 (Linking)
VI  - 27
IP  - 8
DP  - 2001 Dec
TI  - Primary lung fibroblasts from the 129 mouse strain exhibit reduced growth factor 
      responsiveness in vitro.
PG  - 639-53
AB  - Lung fibroblasts are activated to proliferate and produce connective tissue 
      during the development of lung fibrosis. The 129 mouse strain does not develop 
      asbestos-induced fibrogenesis, whereas several other inbred strains rapidly 
      respond to inhaled fibers. Thus, in the experiments presented here, we have 
      compared the responses of primary lung fibroblasts isolated from 129 and C57BL/6 
      mice. The 129 and C57BL/6 mouse lung fibroblasts (MLFs) proliferated similarly in 
      10% fetal bovine serum (FBS), but after quiescence, the 129 MLFs grew more slowly 
      in serum and responded less to the BB isoform of platelet-derived growth factor. 
      This is consistent with our finding that the mRNA for the PDGF-a receptor 
      exhibits reduced expression by the 129 MLFs compared to those from C57BL/6 mice. 
      Fibroblasts from the SJL mouse strain, from a C57BL/6-129 hybrid, and from the 
      3T3 cell line all proliferated more vigorously than MLFs from the 129 mice. In 
      addition, the 129 MLFs exhibited reduced expression of alpha1 procollagen mRNA 
      consequent to treatment with tumor necrosisfactor alpha. Based on these new 
      findings, we suggest that the reduced fibrogenesis in asbestos-exposed 129 mice 
      is due to an intrinsic difference in the ability of the lung fibroblasts to 
      respond to peptide growth factors.
FAU - Brass, D M
AU  - Brass DM
AD  - Department of Pathology, Tulane University Health Sciences Center, New Orleans, 
      Louisiana 70112-2699, USA.
FAU - Tsai, S Y
AU  - Tsai SY
FAU - Brody, A R
AU  - Brody AR
LA  - eng
GR  - R01 HL09242/HL/NHLBI NIH HHS/United States
GR  - R01ES60766/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Exp Lung Res
JT  - Experimental lung research
JID - 8004944
RN  - 0 (Biomarkers)
RN  - 0 (Collagen Type I)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Biomarkers/analysis
MH  - Blotting, Northern
MH  - Cell Count
MH  - Cell Division/drug effects
MH  - Collagen Type I/genetics/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Fibroblasts/cytology/drug effects
MH  - Immunohistochemistry
MH  - Lung/cytology/*drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Platelet-Derived Growth Factor/genetics/*pharmacology
MH  - RNA, Messenger/metabolism
MH  - Receptor, Platelet-Derived Growth Factor alpha/biosynthesis/genetics
MH  - Species Specificity
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Up-Regulation/drug effects/genetics
EDAT- 2002/01/05 10:00
MHDA- 2002/05/03 10:01
CRDT- 2002/01/05 10:00
PHST- 2002/01/05 10:00 [pubmed]
PHST- 2002/05/03 10:01 [medline]
PHST- 2002/01/05 10:00 [entrez]
AID - 10.1080/019021401317138450 [doi]
PST - ppublish
SO  - Exp Lung Res. 2001 Dec;27(8):639-53. doi: 10.1080/019021401317138450.