MXRA7 is involved in megakaryocyte differentiation and platelet production.

IF 1.5 Q3 HEMATOLOGY 血液科学(英文) Pub Date : 2023-07-01 DOI:10.1097/BS9.0000000000000167
Zhenjiang Sun, Benfang Wang, Ying Shen, Kunpeng Ma, Ting Wang, Yiqiang Wang, Dandan Lin
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Abstract

Matrix remodeling is a critical process in hematopoiesis. The biology of MXRA7, as a matrix remodeling associated gene, has still not been reported in hematopoietic process. Public databases showed that MXRA7 expressed in hematopoietic stem cells, suggesting that it may be involved in hematopoiesis. We found that the amounts of megakaryocytes were lower in bone marrow and spleen from Mxra7-/- mice compared with that from wild-type mice. Knock-out of MXRA7 also reduced the amount of platelet in peripheral blood and affected the function of platelets. Knock-out of MXRA7 inhibited hematopoietic stem/progenitor cells differentiate to megakaryocytes possibly through down-regulating the expression of GATA-1 and FOG-1. Moreover, knockdown of MXRA7 in MEG-01 cells could inhibit the cell proliferation and cell apoptosis. Knockdown of MXRA7 inhibited the differentiation of MEG-01 cells and proplatelet formation through suppressing the ERK/MAPK signaling pathway and the expression of β-tubulin. In conclusion, the current study demonstrated the potential significance of MXRA7 in megakaryocyte differentiation and platelet production. The novel findings proposed a new target for the treatment of platelet-related diseases, and much more investigations are guaranteed to dissect the mechanisms of MXRA7 in megakaryocyte differentiation and platelet production.

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MXRA7参与巨核细胞分化和血小板产生。
基质重塑是造血过程中的一个关键过程。MXRA7作为基质重塑相关基因在造血过程中的生物学研究尚未见报道。公开数据库显示MXRA7在造血干细胞中表达,提示其可能参与造血。我们发现,与野生型小鼠相比,Mxra7-/-小鼠骨髓和脾脏中巨核细胞的数量较低。敲除MXRA7后,外周血中血小板数量减少,血小板功能受到影响。敲除MXRA7可能通过下调GATA-1和fog1的表达抑制造血干细胞/祖细胞向巨核细胞的分化。此外,MXRA7在MEG-01细胞中表达下调可抑制细胞增殖和细胞凋亡。MXRA7的下调通过抑制ERK/MAPK信号通路和β-微管蛋白的表达,抑制MEG-01细胞的分化和血小板前形成。总之,本研究证明了MXRA7在巨核细胞分化和血小板产生中的潜在意义。这些新发现为血小板相关疾病的治疗提供了新的靶点,并保证更多的研究可以深入探讨MXRA7在巨核细胞分化和血小板产生中的机制。
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CiteScore
1.70
自引率
0.00%
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0
审稿时长
10 weeks
期刊最新文献
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