BioProject

We investigated the efficacy of sodium thiosulfate (STS) in treating hyperglycemia-induced pronephros damage in zebrafish to gain insights into the underlying mechanisms. More...

We investigated the efficacy of sodium thiosulfate (STS) in treating hyperglycemia-induced pronephros damage in zebrafish to gain insights into the underlying mechanisms. Our results demonstrate that STS treatment effectively restored pronephros damage induced by hyperglycemia. Hyperglycemia was induced in zebrafish by suppressing the pdx1 transcription factor, which plays a crucial role in maintaining physiological pancreatic function. The pronephros structure was analyzed at 48 hours post-fertilization (hpf). Metabolomic profiling and RNA sequencing were conducted on groups subjected to various STS concentrations. Our findings reveal a downregulation of nitric oxide (NO) signaling in zebrafish with a knocked-down pdx1 gene, both metabolomically and transcriptionally. Notably, treatment with STS led to a compensatory upregulation of NO signaling, as evidenced by preliminary metabolomic data, ultimately resulting in the rescue of the pronephros structure. Overall design: To analyze transcriptomic adaptations to STS, RNA-seq of hyperglycemic zebrafish treated with 0 mM, 15 mM, and 20 mM STS was conducted. Zebrafish from a control group exposed to the same STS concentrations were analyzed simultaneously. Hyperglycemia in zebrafish was induced via morpholino technology targeting the transcription factor pdx1, which is responsible for physiological pancreatic development. A control morpholino was injected into zebrafish of the control group. RNA was isolated at 48 hpf. The transgenic zebrafish line Tg(wt1b:EGFP) was used for experimental procedure. Next to RNA-seq analysis, a metabolomic profiling of similar experimental groups was performed. Less...