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Congenital asplenia impairs heme-iron recycling during erythropoiesis in zebrafish

文献类型： 外文期刊

作者： Xie, Lang 1 ; Tao, Yixi 2 ; Shen, Ziwei 1 ; Deng, Huatang 1 ; Duan, Xinbin 1 ; Xue, Yang 3 ; Chen, Daqing 1 ; Li, Yun 2 ;

作者机构： 1.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Natl Agr Sci Observing & Expt Stn Chongqing, Wuhan 430223, Hubei, Peoples R China

2.Southwest Univ, Aquaculture Engn Technol Res Ctr, Coll Fisheries, Chongqing 400715, Peoples R China

3.Chongqing Fisheries Tech Extens Ctr, Chongqing 400020, Peoples R China

关键词： Congenital asplenia; Heme-iron recycling; Erythropoiesis; Zebrafish

期刊名称：DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY （ 影响因子：2.9； 五年影响因子：3.1 ）

ISSN： 0145-305X

年卷期： 2024 年 151 卷

页码：

收录情况： SCI

摘要： The spleen is postulated to be a hematopoietic tissue in adult fish; however, clear evidence is still lacking to define its role in hematopoietic activity. In our previous study, a congenitally asplenic zebrafish was generated though gene editing, which provided a new perspective for studying the role of fish spleen in hematopoiesis. In this study, HSC-regulated and erythrocyte marker genes, such as gata1a, gata2, klf1, hbaa1, hbaa2, hbba1 and hbba2 were significantly reduced in congenitally asplenic zebrafish when compared with wild-type (WT). Sub-sequently, we conducted the transcriptome profiles of whole kidneys from WT and congenitally asplenic zebrafish to explore the possible molecular mechanisms underlying the impaired erythropoiesis caused by congenital asplenia. Our results demonstrated that congenital asplenia might impair heme-iron recycling during erythropoiesis, as evidenced by significant down-regulation of genes associated with iron acquisition (tfr1a, tfa, steap3 and slc25a37) and heme biosynthesis and transport (alas2, fech, uros, urod, copx, ppox and abcb10) in congenitally asplenic zebrafish. In addition, the down-regulation of hemopoiesis-related GO terms, including heme binding, tetrapyrrole binding, iron ion binding, heme metabolic process, heme biosynthetic process, erythrocyte differentiation, iron ion homeostasis and hemoglobin metabolic process confirmed the impaired erythropoiesis induced by congenital asplenia. Our study provides an in-depth understanding of spleen function in regulating heme-iron homeostasis during hematopoiesis, thereby providing valuable insights into pathological responses in splenectomized or congenitally asplenic patients.

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