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The effect of sodium thiosulfate on hyperglycemic zebrafish larvae

ABSTRACT: 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.

ORGANISM(S): Danio rerio

PROVIDER: GSE272119 | GEO | 2024/09/13

REPOSITORIES: GEO

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Project description:Injuries of the zebrafish kidney are rapidly repaired by a migratory response in two to three day-old embryos. While this migratory repair process re-establishes the integrity of the pronephric tubules independently of proliferation, fluid flow, intact cilia, or Wnt signaling, pronephros injuries before 36 hours post fertilization were repaired by a purse string-like mechanism that irreversibly occluded the pronephric tubules. Comparing the gene expression profiles between these two developmental stages and focusing on up-regulated zebrafish pronephros genes, we identified cxcl12a and myca as potential candidates orchestrating the migratory repair process. Zebrafish lines with either cxcl12a or cxcr4b mutations displayed striking repair abnormalities, confirming the requirement for cxc12a/cxcr4b signaling to override the ongoing collective cell migration and repair the pronephros injury. However, in contrast to the collective cell migration of the posterior lateral line primordium, cxc12a/cxcr4b signaling was dispensable for normal pronephros development. Zebrafish myca, the pronephros-specific homologue of human MYC, was also increased in cells participating in the repair response. The defective repair response caused by knockdown of myca resembled the abnormalities observed in cxcx12a/cxcr4b-deficient zebrafish, and was partially rescued by cxcr4b mRNA, suggesting that myca acts in part through up-regulating cxcr4b expression during the migration-based repair process. Kidney-specific knockout of Cxcl12 and Myc suppressed mitochondrial functions, reduced retinoic acid receptor signaling, and delayed the recovery after ischemic/reperfusion injury in mice. Tretinoin, known to stimulate Cxcr4 expression and mitochondrial metabolism, accelerated renal recovery. Thus, the zebrafish pronephros injury mode provides a systematic approach to identify molecules involved in the immediate repair response after kidney injury, and to design strategies to ameliorate this severe complication of human disease.

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The effect of sodium thiosulfate on hyperglycemic zebrafish larvae

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