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(American Journal of Pathology. 1998;153:833-844.)
© 1998 American Society for Investigative Pathology

Regular Articles

Gelatinases A and B Are Up-Regulated in Rat Lungs by Subacute Hyperoxia

Pathogenetic Implications

Annie Pardo* , Roberto Barrios{dagger} , Vilma Maldonado{ddagger} , Jorge Meléndez{ddagger} , Julia Pérez§ , Víctor Ruiz¶ , Lourdes Segura-Valdez¶ , J. Iasha Sznajder|| and Moisés Selman¶

From the Facultad de Ciencias,* UNAM, Coyoacán, México; Department of Pathology,{dagger} Baylor College of Medicine, Houston Texas; Michael Reese Hospital,|| University of Illinois at Chicago, Chicago, Illinois; UAM,§ Unidad Xochimilco; Instituto Nacional de Cancerología,{ddagger} 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-{kappa}ß activation was explored. Oxidative stress significantly increased the lung expression of nuclear transcription factor-{kappa}ß (p65) protein, and nuclear transcription factor-{kappa}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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