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By RT-u2010qPCR and RNAScope, gene expression of genes involved in polyamine homeostasis in various models of acute and chronic kidney injury were examined in polyamine homeostasis. We used mouse embryonic kidney explants as a test for increased Aoc1 expression. However, hypoxia did not lead to changes of Aoc1 expression in vivo. Hyperosmolarity was reported as a result by using the kidney cell lines M15 and 209/MDCT as well as cultured primary proximal tubules. We could show that the rise in Aoc1 expression is related to mRNA-u2010stabilization and transcriptional activation of one specific isoform by using reporter gene and RNA-u2010stability assays. Different models of kidney injury follow a similar pattern of dysregulation of the polyamine system, with the most notable improvement being the introduction of Aoc1 in proximal tubules. "Under harmful conditions," we first offer first insight into the regulation of Aoc1 under inflammatory conditions by using hyperosmolarity as a stimulus.
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