Genetic targets of hydrogen sulfide in ventilator-induced lung injury. Mus musculus

In this study we provide evidence on potential mechanisms involved in H2S mediated protection against VILI. H2S down-regulates genes that are involved in oxidative stress and pro-inflammatory cell responses. H2S regulates ECM remodelling, a mechanism which may contribute to H2S-mediated lung protection. In addition, H2S inhalation activates anti-apoptotic and anti-inflammatory genes, and genes controlling the vascular permeability. The functional relevance of Atf3 underscores the potential of H2S to limit lung injury. We utilized a microarray approach for large scale analysis of target genes in order to elucidate the therapeutic effects of H2S in VILI. This study demonstrates the influence of supplemental H2S on gene expression in a model of VILI. In addition to describing the genes differentially regulated in VILI, the present study focused on newly identified H2S target genes within several functional groups, including anti-inflammatory and anti-apoptotic pathways, regulation of extracellular matrix (ECM) remodelling and angiogenesis. Overall design: Gene expression analysis of control group, allowed to breathe spontaneously synthetic air and mice ventilated with synthetic air or synthetic air with 80 ppm H2S for 6 hours.