ArticleMolecular biology reports2012
Microarray analysis of differentially expressed background genes in rats following hemorrhagic shock.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Endothelial cell-derived SSAO can increase MLCOpen life sciences · 2021Article
- Hypoxia serves a key function in the upregulated expression of vascular adhesion protein‑1 in vitro and in a rat model of hemorrhagic shock.Molecular medicine reports · 2017Article
- Aldehyde dehydrogenases in cellular responses to oxidative/electrophilic stress.Free radical biology & medicine · 2013Review
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4 authors at 1 institution in 1 country.
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Abstract
To uncover the contribution of the diversity of the genetic backgrounds to the pathogenesis of hemorrhagic shock, we employed male Sprague-Dawley rats to establish a controlled 2.5 ml/100 g total body weight fixed-volume hemorrhagic shock and left lobular hepatectomy model. RNA was isolated from the liver samples taken from the rats (survival group: rats survived over 24 h after shock; and dead group: rats died within 1 h after shock, n = 3 per group), and subjected to microarray using the illumina(TM) chips for rat cDNA (27,342 genes, >700,000 probes). The results demonstrated that the rats had about 50% survival rate and 100 genes were identified differentially expressed in the two groups. Of these genes, 47 genes were up-regulated and 53 genes down-regulated. Real-time PCR confirmed the differential expression for Aldh1a1, Aldh1a7, Aoc3, Cyp26al, Hdc and Ephx2 genes. Pathway analysis revealed that these genes are involved in circadian rhythm, beta-Alanine metabolism, histidine metabolism, biosynthesis of unsaturated fatty acids, glycine, serine and threonine metabolism, vitamin B6 metabolism, as well as arginine and proline metabolism. Therefore, our study provided a global molecular view on the contribution of genetic backgrounds to the response to hemorrhagic shock.
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