TY - JOUR
T1 - The in vitro protection of human decay accelerating factor and hDAF/heme oxygenase-1 transgenes in porcine aortic endothelial cells against sera of formosan macaques
AU - Tu, C. F.
AU - Tai, H. C.
AU - Wu, C. P.
AU - Ho, L. L.
AU - Lin, Y. J.
AU - Hwang, C. S.
AU - Yang, T. S.
AU - Lee, J. M.
AU - Tseng, Y. L.
AU - Huang, C. C.
AU - Weng, C. N.
AU - Lee, P. H.
N1 - Funding Information:
Supported by grants from the National Science Council ( NSC 90-2313-B-059-007 , NSC 91-2313-B-059-001 , and NSC 92-2313-B-059-002 ) of Executive Yung, Taiwan, ROC.
Copyright:
Copyright 2011 Elsevier B.V., All rights reserved.
PY - 2010/7
Y1 - 2010/7
N2 - To mitigate hyperacute rejection, pigs have been generated with α-Gal transferase gene knockout and transgenic expression of human decay accelerating factor (hDAF), MCP, and CD59. Additionally, heme-oxygenase-1 (HO-1) has been suggested to defend endothelial cells. Sera (MS) (0%, 1%, 5%, 10%, and 15%) from Formosan macaques (Macaca cyclopis, MC), an Old World monkey wildly populated in Taiwan, was used to test the protective in vitro, effects of hDAF or hDAF/hHO-1 on porcine aortic endothelial cells (pAEC) derived from hDAF +, hDAF+/hHO-1+, and hDAF+/hHO- 1- and 1 nontransgenic pAEC. Ten percent human serum (HS) served as a positive control. When MS addition increased to 10% or 15%, all transgenic pAEC exhibited a greater survival than nontransgenic pAEC. Noticeably, 15% MS reduced survived to <10% versus >40% in nontransgenic and transgenic pAEC, respectively. These results revealed that hDAF exerted protective effects against MC complement activation. However, comparing with 10% MS and HS in pAEC of nontransgenic pigs, the survivability was higher in HS, suggesting that complement activation by MS was more toxic than that by HS. Furthermore, hDAF+/hHO-1+ showed no further protection against effects of MS on transgenic pAEC.
AB - To mitigate hyperacute rejection, pigs have been generated with α-Gal transferase gene knockout and transgenic expression of human decay accelerating factor (hDAF), MCP, and CD59. Additionally, heme-oxygenase-1 (HO-1) has been suggested to defend endothelial cells. Sera (MS) (0%, 1%, 5%, 10%, and 15%) from Formosan macaques (Macaca cyclopis, MC), an Old World monkey wildly populated in Taiwan, was used to test the protective in vitro, effects of hDAF or hDAF/hHO-1 on porcine aortic endothelial cells (pAEC) derived from hDAF +, hDAF+/hHO-1+, and hDAF+/hHO- 1- and 1 nontransgenic pAEC. Ten percent human serum (HS) served as a positive control. When MS addition increased to 10% or 15%, all transgenic pAEC exhibited a greater survival than nontransgenic pAEC. Noticeably, 15% MS reduced survived to <10% versus >40% in nontransgenic and transgenic pAEC, respectively. These results revealed that hDAF exerted protective effects against MC complement activation. However, comparing with 10% MS and HS in pAEC of nontransgenic pigs, the survivability was higher in HS, suggesting that complement activation by MS was more toxic than that by HS. Furthermore, hDAF+/hHO-1+ showed no further protection against effects of MS on transgenic pAEC.
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U2 - 10.1016/j.transproceed.2010.05.104
DO - 10.1016/j.transproceed.2010.05.104
M3 - Article
C2 - 20692427
AN - SCOPUS:77955535896
SN - 0041-1345
VL - 42
SP - 2138
EP - 2141
JO - Transplantation Proceedings
JF - Transplantation Proceedings
IS - 6
ER -