Israeli, ZeevZeevIsraeli2023-03-162009-02-242023-03-162009http://nbn-resolving.de/urn:nbn:de:hebis:26-opus-68688https://jlupub.ub.uni-giessen.de/handle/jlupub/14015http://dx.doi.org/10.22029/jlupub-13397Hypoxia is known to trigger inflammatory reaction solely or in concert with other stimuli leading to lung damage. Hypoxia- induced lung damage is mediated by the secretion of pro-inflammatory cytokines by alveolar macrophages (AM). To learn more about the genes involved in the hypoxia mediated- activation of AM, m-RNA of AM from mice kept under normoxia/hypoxia for 1 or 21 days was isolated and studied using three established techniques: Microarrays, real-time PCR and immunohistochemistry. Array results confirmed that hypoxia is a mild stimulus for macrophages; No strongly regulated genes were identified and the expression pattern of selected genes as explored by PCR did not support arrays findings. Immunostaining for two selected genes demonstrated a decrease of vimentin expression under acute hypoxia (1 day) and an increase of integrin b2 expression under chronic hypoxia (21 days).Our findings show that hypoxia is a mild stimulus in AM; identification of genes with mild regulation is difficult so future studies should rely on a considerably larger sample sizes. Regulation was confirmed on protein level by immunohistochemical staining for two selected genes, more studies are needed for validation and better understanding of this phenomena.enIn CopyrightHypoxiagene expresionalveolar macrophagesddc:610