Hyperoxia induces interstitial (type I) and increases type IV collagenase mRNA expression and increases type I and IV collagenolytic activity in newborn rat lung
Autor: | R. Govindrajan, Milagros Malicdem, Uday P. Devaskar, Wiley Taylor, Sarah Heyman, Daphne E. deMello |
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Rok vydání: | 1994 |
Předmět: |
Pathology
medicine.medical_specialty Neutrophils Gene Expression Pulmonary Edema Lung injury Biology Hyperoxia Basement Membrane Rats Sprague-Dawley Body Water medicine Animals Collagenases RNA Messenger Oxygen toxicity Lung chemistry.chemical_classification Reactive oxygen species Macrophages Neutrophil collagenase respiratory system medicine.disease Pulmonary edema Molecular biology Rats Microscopy Electron chemistry Animals Newborn Matrix Metalloproteinase 9 Pediatrics Perinatology and Child Health Collagenase Interstitial collagenase medicine.symptom Matrix Metalloproteinase 1 Developmental Biology medicine.drug |
Zdroj: | Biology of the neonate. 66(2-3) |
ISSN: | 0006-3126 |
Popis: | Oxygen toxicity is attributed to the reaction of oxygen metabolites with cellular components leading to cell destruction. Activation of latent human neutrophil interstitial collagenase by reactive oxygen species has been demonstrated. The potential role of collagenases in hyperoxic lung injury has not been investigated. We studied the effect of hyperoxia on newborn rat lung water content, morphology and ultrastructure, interstitial (type I) and type IV collagenase gene expression and type I and IV collagenolytic activity. We observed that hyperoxia causes pulmonary edema, alters newborn rat lung morphology in a sequential manner and produces ultrastructural alterations, induces type I and increases type IV collagenase mRNA expression, and increases type I and IV collagenolytic activity. A role for type I and IV collagenase in hyperoxic newborn lung injury or in the recovery following the injury is proposed. |
Databáze: | OpenAIRE |
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