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Medical Research Council Group in Lung Development and Lung Biology Research Program, Hospital for Sick Children Research Institute, University of Toronto, Toronto, Ontario, Canada M5G 1X8
We have previously
shown that an intermittent mechanical strain regimen (5% elongation,
60 cycles/min, 15 min/h) that simulates fetal breathing movements
stimulated fetal rat lung cell proliferation. Because normal lung
growth requires proper coordination between cell proliferation and
extracellular matrix (ECM) remodeling, we subjected organotypic
cultures of fetal rat lung cells (day 19 of gestation, term = 22 days) to
this strain regimen and examined alterations in ECM gene and protein
expression. Northern analysis revealed that mechanical strain reduced
messages for procollagen-
1(I) and biglycan and increased the levels of mRNA for
collagen-1(IV) and
-2(IV), whereas laminin
-chain mRNA levels remained constant. Regardless of mRNA changes,
mechanical strain increased the protein content of type I and type IV
collagen as well as of biglycan in the medium. Mechanical strain did
not affect gene expression of several matrix metalloproteinases (MMPs),
such as MMP-1 (interstitial collagenase), MMP-2 (gelatinase A), and
MMP-3 (stromelysin-1). Neither collagenase nor gelatinase (A and B)
activities in conditioned medium were affected by mechanical strain.
Tissue inhibitor of metalloproteinase activities in conditioned medium
remained unchanged during the 48-h intermittent mechanical stretching.
These data suggest that an intermittent mechanical strain
differentially regulates gene and protein expression of ECM molecules
in fetal lung cells. The observed increase in matrix accumulation
appears to be mainly a result of an increased synthesis of ECM
molecules and not of decreasing activity of degradative enzymes.
fetal lung development; matrix metalloproteinases; gene expression; protein synthesis
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