Affiliations: [a] Department of Urology, Capital Medical University, Beijing Friendship Hospital, Beijing, China | [b] State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China | [c] Hemorheology Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China | [d] Department of Urology, 309th Hospital of PLA, Beijing, China
Correspondence:
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Corresponding author: Ye Tian, Capital Medical University, Beijing Friendship Hospital, Beijing 100050, China. Tel.: +86 10 63138370; Fax: +86 10 83161939; E-mail: [email protected].
Correspondence:
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Corresponding author: Weijuan Yao, Hemorheology Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. Tel.: +86 10 82802419; Fax: +86 10 62015582; E-mail: [email protected].
Abstract: Living-donor renal transplantation is an ideal treatment for patients with end stage renal disease because it affords earlier transplantation and better graft for long term survival. CD14+ monocytes are the predominant inflammatory cells in renal allograft intimal arteritis. The biomechanical alterations in CD14+ monocytes would affect the function of graft. The aim of the present study was to explore the changes in the biorheological properties of CD14+ monocytes before and after the living donor renal transplantation. We found that the viscoelastic properties of CD14+ monocytes were greatly decreased after renal transplantation. Confocal microscopy showed that the F-actin content was increased when the oral immunosuppressive agents started. We also found that two cytoskeletal regulatory proteins, cofilin1 and profilin1, changed. Our results suggest that the immunosuppressive agents could significantly change the biorheological characteristics of the CD14+ mononuclear cells and the biomechanical changes may greatly affects their function, which would play a critical role to gain longer immune-tolerance stage.
