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Updated: Feb 11, 2026
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Synthesis of Monocyte-targeting Peptide Amphiphile Micelles for Imaging of Atherosclerosis
Published on: November 17, 2017
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ST6GAL1 negatively regulates monocyte transendothelial migration and atherosclerosis development
Jun Zhang1, Yan Liu1, Xiao Deng1
1Institute of Life Sciences, College of Pharmacy, Chongqing Medical University, No.1 Yixueyuan Road, Yuzhong District, Chongqing 400016, PR China.
Biochemical and Biophysical Research Communications
|April 15, 2018
Summary
Alpha-2,6 sialyltransferase 1 (ST6GAL1) expression decreases in atherosclerosis. Restoring ST6GAL1 inhibits monocyte migration and may prevent atherosclerosis by sialylating beta-catenin.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Glycobiology
Background:
- Monocyte transendothelial migration is a key early event in atherosclerosis.
- The role of alpha-2,6 sialyltransferase 1 (ST6GAL1) in atherosclerosis is increasingly recognized but not fully understood.
Purpose of the Study:
- To investigate the direct relationship between ST6GAL1 expression and atherosclerosis.
- To elucidate the mechanism by which ST6GAL1 influences monocyte migration.
Main Methods:
- Quantitative analysis of ST6GAL1 expression during atherosclerosis development and regression.
- RNA interference and overexpression studies in EA.hy926 endothelial cells to assess ST6GAL1's effect on monocyte migration.
- Identification and analysis of beta-catenin sialylation in response to TNFα stimulation.
Main Results:
- ST6GAL1 expression was significantly reduced during atherosclerosis development and increased upon regression.
- Knockdown of ST6GAL1 promoted TNFα-induced monocyte migration, while overexpression inhibited it.
- Beta-catenin was identified as a sialylated protein, with decreased sialylation observed in TNFα-treated cells.
Conclusions:
- ST6GAL1 plays a protective role against atherosclerosis by inhibiting monocyte transendothelial migration.
- The mechanism may involve the sialylation of endothelial beta-catenin.
- ST6GAL1 represents a potential therapeutic target for atherosclerosis prevention and treatment.
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