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首页|期刊导航|中国输血杂志|基于MEG-01细胞模型探究低水平ST6Gal-Ⅰ介导CD36去唾液酸化在ITP中的潜在机制

基于MEG-01细胞模型探究低水平ST6Gal-Ⅰ介导CD36去唾液酸化在ITP中的潜在机制

范娜 钟磊 刘雯 佟安琪 梁静

中国输血杂志2025,Vol.38Issue(9):1162-1166,5.
中国输血杂志2025,Vol.38Issue(9):1162-1166,5.DOI:10.13303/j.cjbt.issn.1004-549x.2025.09.006

基于MEG-01细胞模型探究低水平ST6Gal-Ⅰ介导CD36去唾液酸化在ITP中的潜在机制

Investigating the role of low-level ST6Gal-Ⅰ-mediated CD36 desialylation in ITP based on the MEG-01 cell model

范娜 1钟磊 2刘雯 1佟安琪 3梁静1

作者信息

  • 1. 新疆医科大学第六附属医院,新疆 乌鲁木齐 830002
  • 2. 新疆维吾尔自治区儿童医院,新疆 乌鲁木齐 830000
  • 3. 新疆医科大学第七附属医院,新疆 乌鲁木齐 830017
  • 折叠

摘要

Abstract

Objective To investigate the correlation among α2,6-sialyltransferase(ST6Gal-Ⅰ),CD36 desialylation,and caveolin-1(Cav-1)in phorbol ester(PMA)-induced MEG-01 cell model,as well as their potential mechanism in im-mune thrombocytopenia(ITP).Methods MEG-01 cells were treated with 10 ng/mL PMA for 48 hours(control group:0.1%DMSO).Flow cytometry was used to detect cell surface markers:desialylation(CD41+RCA+)and α2,6-sialylation(CD41+SNA+).Western blot was performed to analyze the protein expressions of ST6Gal-Ⅰ,CD36,and Cav-1.Results Flow cytometry analysis revealed that,compared with the control group(set as 100%),the proportion of CD41+RCA+posi-tive cells in the MEG-01 cells after PMA intervention significantly increased to(127.79±2.01)%,while the proportion of CD41+SNA+positive cells significantly decreased to(78.09±1.76)%(both P<0.05).Western blot analysis results showed that,compared with the control group,PMA intervention significantly downregulated the expression of ST6Gal-Ⅰ protein(0.602±0.023 vs 0.768±0.068)and Cav-1 protein(1.012±0.028 vs 1.253±0.068)(both P<0.05),while significant-ly upregulating the expression of CD36 protein(0.936±0.033 vs 0.694±0.070,P<0.05).Conclusion PMA can signifi-cantly inhibit the expression of ST6Gal-Ⅰ,accompanied by increased desialylation(β-galactose exposure),elevated CD36,and downregulated Cav-1.These changes suggest that the increased exposure of CD36 antigen and the disorder of membrane microenvironment may be involved in the pathological process of ITP,providing a new direction for mechanism research.

关键词

免疫性血小板减少症/CD36/去唾液酸化/α2,6唾液酸转移酶Ⅰ/小窝蛋白-1

Key words

immune thrombocytopenia/CD36/desialylation/ST6Gal-Ⅰ/Caveolin-1

分类

医药卫生

引用本文复制引用

范娜,钟磊,刘雯,佟安琪,梁静..基于MEG-01细胞模型探究低水平ST6Gal-Ⅰ介导CD36去唾液酸化在ITP中的潜在机制[J].中国输血杂志,2025,38(9):1162-1166,5.

基金项目

新疆医科大学自然科学青年研究项目(2024XYZR52) (2024XYZR52)

"天山英才"医药卫生高层次领军人才培养计划(TSYC202301A044) (TSYC202301A044)

新疆医科大学科第六附属医院科研创新基金(LFYKYZX2023-09) (LFYKYZX2023-09)

中国输血杂志

1004-549X

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