Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes
Abnormal adhesion of red blood cells (RBC) to the endothelium has been linked to the pathophysiology of several diseases associated with vascular disorders. Various biochemical changes on the outer membrane of RBC, as well as plasma protein levels, have been identified as possibly playing key roles,...
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sg-ntu-dr.10356-1515212021-06-18T02:38:58Z Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes Kaliyaperumal, Rani Deng, Xiaopeng Meiselman, Herbert J. Song, Hao Dalan, Rinkoo Leow, Melvin Khee-Shing Neu, Björn Lee Kong Chian School of Medicine (LKCMedicine) School of Chemical and Biomedical Engineering Tan Tock Seng Hospital Duke-NUS Medical School Science::Medicine Red Blood Cell Nonreactive Polymers Abnormal adhesion of red blood cells (RBC) to the endothelium has been linked to the pathophysiology of several diseases associated with vascular disorders. Various biochemical changes on the outer membrane of RBC, as well as plasma protein levels, have been identified as possibly playing key roles, but the detailed interplay between plasma factors and cellular factors often remains unclear. In this work, we identified an alternative pathway by demonstrating that non-adsorbing macromolecules can also have a marked impact on the adhesion efficiency of RBC from patients with type 2 Diabetes (T2DM) to endothelial cells (EC). RBC isolated from blood samples of T2DM patients were suspended in isotonic solutions of dextran in order to mimic the impact of non-adsorbing macromolecules. Static and continuous flow adhesion assays were used to determine the adhesion behavior of T2DM RBC with EC and the results compared with those of normal controls. We found that the presence of non-adsorbing molecules promotes an increase in T2DM RBC - EC adhesion and that these RBC exhibit much greater adhesion than normal red cells. Our results thus suggest that the depletion mechanism might be an alternative phenomenon through which plasma proteins could cause enhanced RBC-EC adhesion in diabetes mellitus. These findings contribute towards the comprehensive understanding of pathophysiological mechanisms of vascular complications in diabetes and other diseases with similar vascular sequelae. Agency for Science, Technology and Research (A*STAR) Ministry of Education (MOE) National Research Foundation (NRF) This work was supported by grants from the Ministry of Education (Singapore), the National Research Foundation (Singapore) and from the Agency for Science, Technology and Research (A*Star, Singapore, BMRC grant 05/1/22/19/382). 2021-06-18T02:38:58Z 2021-06-18T02:38:58Z 2019 Journal Article Kaliyaperumal, R., Deng, X., Meiselman, H. J., Song, H., Dalan, R., Leow, M. K. & Neu, B. (2019). Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes. Biochemical and Biophysical Research Communications, 516(1), 144-148. https://dx.doi.org/10.1016/j.bbrc.2019.06.018 0006-291X https://hdl.handle.net/10356/151521 10.1016/j.bbrc.2019.06.018 31200959 2-s2.0-85066947364 1 516 144 148 en 05/1/22/19/382 Biochemical and Biophysical Research Communications © 2019 Elsevier Inc. All rights reserved. |
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Science::Medicine Red Blood Cell Nonreactive Polymers Kaliyaperumal, Rani Deng, Xiaopeng Meiselman, Herbert J. Song, Hao Dalan, Rinkoo Leow, Melvin Khee-Shing Neu, Björn Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
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Abnormal adhesion of red blood cells (RBC) to the endothelium has been linked to the pathophysiology of several diseases associated with vascular disorders. Various biochemical changes on the outer membrane of RBC, as well as plasma protein levels, have been identified as possibly playing key roles, but the detailed interplay between plasma factors and cellular factors often remains unclear. In this work, we identified an alternative pathway by demonstrating that non-adsorbing macromolecules can also have a marked impact on the adhesion efficiency of RBC from patients with type 2 Diabetes (T2DM) to endothelial cells (EC). RBC isolated from blood samples of T2DM patients were suspended in isotonic solutions of dextran in order to mimic the impact of non-adsorbing macromolecules. Static and continuous flow adhesion assays were used to determine the adhesion behavior of T2DM RBC with EC and the results compared with those of normal controls. We found that the presence of non-adsorbing molecules promotes an increase in T2DM RBC - EC adhesion and that these RBC exhibit much greater adhesion than normal red cells. Our results thus suggest that the depletion mechanism might be an alternative phenomenon through which plasma proteins could cause enhanced RBC-EC adhesion in diabetes mellitus. These findings contribute towards the comprehensive understanding of pathophysiological mechanisms of vascular complications in diabetes and other diseases with similar vascular sequelae. |
author2 |
Lee Kong Chian School of Medicine (LKCMedicine) |
author_facet |
Lee Kong Chian School of Medicine (LKCMedicine) Kaliyaperumal, Rani Deng, Xiaopeng Meiselman, Herbert J. Song, Hao Dalan, Rinkoo Leow, Melvin Khee-Shing Neu, Björn |
format |
Article |
author |
Kaliyaperumal, Rani Deng, Xiaopeng Meiselman, Herbert J. Song, Hao Dalan, Rinkoo Leow, Melvin Khee-Shing Neu, Björn |
author_sort |
Kaliyaperumal, Rani |
title |
Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
title_short |
Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
title_full |
Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
title_fullStr |
Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
title_full_unstemmed |
Depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
title_sort |
depletion interaction forces contribute to erythrocyte-endothelial adhesion in diabetes |
publishDate |
2021 |
url |
https://hdl.handle.net/10356/151521 |
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1703971174746161152 |