Investigating the role of low-level ST6Gal-Ⅰ-mediated CD36 desialylation in ITP based on the MEG-01 cell model
10.13303/j.cjbt.issn.1004-549x.2025.09.006
- VernacularTitle: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
- Author:
Na FAN
1
;
Lei ZHONG
2
;
Wen LIU
1
;
Anqi TONG
3
;
Jing LIANG
1
Author Information
1. The Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi 830002, China
2. Xinjiang Uygur Autonomous Region Children's Hospital, Urumqi 830000, China
3. The Seventh Affiliated Hospital of Xinjiang Medical University, Urumqi 830017, China
- Publication Type:Journal Article
- Keywords:
immune thrombocytopenia;
CD36;
desialylation;
ST6Gal-Ⅰ;
Caveolin-1
- From:
Chinese Journal of Blood Transfusion
2025;38(9):1162-1166
- CountryChina
- Language:Chinese
-
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 immune 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
positive 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 significantly upregulating the expression of CD36 protein (0.936±0.033 vs 0.694±0.070, P<0.05). Conclusion: PMA can significantly 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.
