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From the Facultad de Ciencias,*
UNAM, Coyoacán,
México; Department of Pathology,
Baylor
College of Medicine, Houston Texas; Michael Reese
Hospital,||
University of Illinois at Chicago, Chicago,
Illinois; UAM,§
Unidad Xochimilco; Instituto
Nacional de Cancerología,
and
Instituto Nacional de Enfermedades
Respiratorias,¶
México
Subacute hyperoxia may cause basement membrane disruption and
subsequent fibrosis. To test the role of extracellular matrix
degradation in hyperoxic damage, we analyzed the expression of
gelatinases A and B and tissue inhibitors of metalloproteinases
(TIMP)-1 and TIMP-2 in rats exposed to 85% O2.
Oxygen-exposed rats were studied at 1, 3, 5,
and 7 days, and compared with air-breathing rats. Lung mRNAs
assayed by Northern and in situ hybridization showed an
up-regulation of lung gelatinases A and B from the 3rd day on.
Gelatinase A was localized in alveolar macrophages and in interstitial
and alveolar epithelial cells. Gelatinase B mRNA and protein were
localized in macrophages and bronchiolar and alveolar epithelial cells.
Increased gelatinase A and B activities were demonstrated in
bronchoalveolar lavage. TIMP-1 and TIMP-2 were constitutively
expressed, and only TIMP-1 displayed a moderate increase with
hyperoxia. To elucidate transcriptional mechanisms for increased
gelatinase B expression after hyperoxia, nuclear transcription
factor-
ß activation was explored. Oxidative stress significantly
increased the lung expression of nuclear transcription factor-ß
(p65) protein, and nuclear transcription factor-ß
activation and increased levels of gelatinases A and B were found in
isolated type II alveolar cells obtained from hyperoxic rats.
Conceivably, subacute hyperoxia induces excessive gelatinase
activity, which may contribute to lung damage.
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