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TNF-α pretreated hematopoietic stem cells inhibit the migration and inflammatory response of HUVECs and attenuate GVHD

干细胞 川地34 造血 肿瘤坏死因子α 趋化因子 细胞凋亡 MMP9公司 免疫学 癌症研究 CXCR4型 MMP2型 生物 炎症 细胞生物学 下调和上调 生物化学 基因
作者
Jilei Sun,Tingting Zhou,Shiyuan Qin,Yaolei Zhang,Yong Yang,Zhitao Wei
出处
期刊:Current stem cell research & therapy [Bentham Science]
卷期号:18
标识
DOI:10.2174/1574888x18666230731150317
摘要

Background: Hematologic diseases have seriously threatened human health. Although hematopoietic stem cell transplantation (HSCT) is an effective curative option, the complications, especially graft-versus-host disease (GVHD), are a big problem. Methods: TNF-α pretreatment of hematopoietic stem cells. Apoptosis was detected by flow cytometry, Transwell, and wound healing assays were used to assess cell migration and invasion, E-selectin expression was observed by fluorescence imaging, the levels of NO were measured by a kit, the expression of E-cadherin, MMP2, and MMP9 was detected in cells by qRT-PCR, and western blot was used to analyze the expression of E-cadherin, CXCL12, MCP-1, MCP-3, MMP2, and MMP9. Results: TNF-α induces a high apoptosis rate of CD3, CD19, and CD133 and a low apoptosis rate of CD34. The level of Fas and TNF-R1 was significantly high than that of TNF-R2. HSCs treated with TNF-α declined the invasion and migration of HUVECs. E-selectin, MMP2 and MMP9 mRNA levels of HUVECs and MMP2, CXCL12, MCP-1, and MCP-3 were decreased after HSCs-TNF-α treatment, while the E-cadherin mRNA and protein level of HUVECs was enhanced with HSCs-TNF-α treatment. Conclusion: TNF-α pretreated HSCs can lead to reduced levels of migration, adhesion, and chemokines of HUVECs, thereby declining the inflammatory response and GVHD.
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