Document Type
Article
Publication Date
9-1-2015
Publication Title
Glycobiology
Abstract
Sialic acids (SAs) are widely expressed on immune cells and their levels and linkages named as sialylation status vary upon cellular environment changes related to both physiological and pathological processes. In this study, we performed a global profiling of the sialylation status of macrophages and their release of SAs in the cell culture medium by using flow cytometry, confocal microscopy and liquid chromatography tandem mass spectrometry (LC-MS/MS). Both flow cytometry and confocal microscopy results showed that cell surface α-2,3-linked SAs were predominant in the normal culture condition and changed slightly upon treatment with atorvastatin for 24 h, whereas α-2,6-linked SAs were negligible in the normal culture condition but significantly increased after treatment. Meanwhile, the amount of total cellular SAs increased about three times (from 369 ± 29 to 1080 ± 50 ng/mL) upon treatment as determined by the LC-MS/MS method. On the other hand, there was no significant change for secreted free SAs and conjugated SAs in the medium. These results indicated that the cell surface α-2,6 sialylation status of macrophages changes distinctly upon atorvastatin stimulation, which may reflect on the biological functions of the cells.
Recommended Citation
Wang, Dan; Nie, Huan; Ozhegov, Evgeny; Wang, Lin; Zhou, Aimin; Li, Yu; and Sun, Xue Long, "Globally Profiling Sialylation Status of Macrophages Upon Statin Treatment" (2015). Chemistry Faculty Publications. 389.
https://engagedscholarship.csuohio.edu/scichem_facpub/389
DOI
10.1093/glycob/cwv038
Version
Postprint
Publisher's Statement
This is a pre-copyedited, author-produced PDF of an article accepted for publication in Glycobiology following peer review. The version of record Wang, D.; Nie, H.; Ozhegov, E.; Wang, L.; Zhou, A.; Li, Y.; Sun, X. Globally profiling sialylation status of macrophages upon statin treatment. Glycobiology 2015, 25, 1007-1015. is available online at: https://doi.org/10.1093/glycob/cwv038
Volume
25
Issue
9
Comments
This work was supported by Faculty Research Development Fund and the research fund from the Center for Gene Regulation in Health and Disease (GRHD) at Cleveland State University supported by Ohio Department of Development (ODOD). The authors acknowledge the National Science Foundation Major Research Instrumentation Grant (CHE-0923398) for supporting Q-Trap 5500 mass spectrometer instrument, the National Institution of Health for supporting Nikon A1Rsi confocal microscope (1S10OD010381). This work was partially supported by grants from The National Natural Science Foundation of China (31328006). H Nie appreciates the China Oversea Scholar Award from China Scholarship Council.