PUBLICATION
The zebrafish caudal fin amputation model simulates the impact of hyperglycemia on inflammation and regeneration
- Authors
- Li, H., Zhao, Y.C., Mo, D.S., Zhang, Y.J., Yang, Y.Z., Huang, J.T., Kong, P., Zhou, T., Lu, H., He, Z.X., Shu, L.P.
- ID
- ZDB-PUB-251121-17
- Date
- 2025
- Source
- American journal of translational research 17: 765976757659-7675 (Journal)
- Registered Authors
- He, Zhi-Xu, Shu, Li-Ping
- Keywords
- Danio rerio, MAPK pathway, hyperglycemia, inflammatory factors, leukocyte migration, tissue repair and regeneration
- MeSH Terms
- none
- PubMed
- 41268230 Full text @ Am J Transl Res
Citation
Li, H., Zhao, Y.C., Mo, D.S., Zhang, Y.J., Yang, Y.Z., Huang, J.T., Kong, P., Zhou, T., Lu, H., He, Z.X., Shu, L.P. (2025) The zebrafish caudal fin amputation model simulates the impact of hyperglycemia on inflammation and regeneration. American journal of translational research. 17:765976757659-7675.
Abstract
Objective In this study, we aimed to create a diabetic zebrafish model and investigate the effects of high glucose levels on both inflammation and tissue regeneration.
Methods We established the Tübingen strain of zebrafish (wild type, WT) and Tg (mpo: EGFP), and Tg (coro1a: EGFP) zebrafish models of caudal fin amputation to study tissue regeneration and assess inflammation.
Results Our results revealed that elevated glucose levels led to the increased recruitment of neutrophils and macrophages following amputation. Zebrafish larvae exposed to 222 mM glucose for 14 days exhibited severely impaired limb regeneration postamputation. In addition, the levels of key inflammatory factors, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1), which are closely associated with the development of diabetic wounds, were significantly increased after caudal fin amputation upon glucose exposure. Most notably, the p38 inhibitor SB203580 effectively reduced the expression of these key inflammatory factors and promoted tissue regeneration under high-glucose conditions. According to high-throughput transcriptome sequencing, caudal fin amputation following glucose exposure resulted in the enrichment of genes in several pathways involved in amino acid metabolism, lipid metabolism, and inflammation.
Conclusions Our study provides a comprehensive genetic and molecular profile that closely recapitulates human diabetes. This system offers a valuable avenue for advancing basic research in the field of inflammation and regeneration within a diabetic context and promotes translational research for diabetes therapy.
Genes / Markers
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Phenotype
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Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping