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

C. F. Tu, H. C. Tai, C. P. Wu, L. L. Ho, Y. J. Lin, C. S. Hwang, T. S. Yang, J. M. Lee, Yau-Lin Tseng, C. C. Huang, C. N. Weng, P. H. Lee

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)2138-2141
Number of pages4
JournalTransplantation Proceedings
Volume42
Issue number6
DOIs
Publication statusPublished - 2010 Jul 1

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CD55 Antigens
Heme Oxygenase-1
Macaca
Transgenes
Swine
Endothelial Cells
Serum
Complement Activation
In Vitro Techniques
Cercopithecidae
Gene Knockout Techniques
Poisons
Transferases
Taiwan

All Science Journal Classification (ASJC) codes

  • Surgery
  • Transplantation

Cite this

Tu, C. F. ; Tai, H. C. ; Wu, C. P. ; Ho, L. L. ; Lin, Y. J. ; Hwang, C. S. ; Yang, T. S. ; Lee, J. M. ; Tseng, Yau-Lin ; Huang, C. C. ; Weng, C. N. ; Lee, P. H. / 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. In: Transplantation Proceedings. 2010 ; Vol. 42, No. 6. pp. 2138-2141.
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abstract = "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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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. / Tu, C. F.; Tai, H. C.; Wu, C. P.; Ho, L. L.; Lin, Y. J.; Hwang, C. S.; Yang, T. S.; Lee, J. M.; Tseng, Yau-Lin; Huang, C. C.; Weng, C. N.; Lee, P. H.

In: Transplantation Proceedings, Vol. 42, No. 6, 01.07.2010, p. 2138-2141.

Research output: Contribution to journalArticle

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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, Yau-Lin

AU - Huang, C. C.

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AU - Lee, P. H.

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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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