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Home > Medicine & Health Science textbooks > Surgery > The Possible Mechanisms of Peroxisome Proliferator-Activated Receptor (Ppar) Agonists in Controlling Graft Rejection
The Possible Mechanisms of Peroxisome Proliferator-Activated Receptor (Ppar) Agonists in Controlling Graft Rejection

The Possible Mechanisms of Peroxisome Proliferator-Activated Receptor (Ppar) Agonists in Controlling Graft Rejection


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About the Book

This dissertation, "The Possible Mechanisms of Peroxisome Proliferator-activated Receptor (PPAR) Agonists in Controlling Graft Rejection" by Qi, Cai, 蔡綺, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled "The Possible Mechanisms of Peroxisome Proliferator-Activated Receptor (PPAR) Agonists in Controlling Graft Rejection" Submitted by Qi CAI for the degree of Master of Philosophy at The University of Hong Kong in August 2005 Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors which regulate gene expression by transactivation and transrepression. PPARs are intensively studied in lipid metabolism and homeostasis. However, our understanding of the regulatory roles of PPARs in inflammation and immune responses is evolving rapidly. Of the three isotypes of the PPAR family (α, β and γ), PPARγ and PPARα have been shown to be important in the regulation of inflammation, immune responses and atherosclerosis. Transplantation is the ultimate choice for patients with end-stage organ failure. The use of T cell activation inhibitors such as cyclosporin A (CsA) has been effective in controlling acute rejection of solid organ transplants. However, chronic graft damage manifested by graft vascular atherosclerosis and interstitial fibrosis is not prevented and remains to be a major problem to achieve long-term graft survival. Previous studies from our group have shown that the PPARγ agonist rosiglitazone (Rosi) significantly prolonged graft survival and reduced the severity of chronic graft damage in a rat cardiac heterotopic transplantation model. To further explore the mechanisms mediated by Rosi in controlling chronic graft damage, cDNA microarray was performed to compare gene expression profile of heart grafts treated with CsA alone or in combination with Rosi. Microarray analysis suggested that Rosi might benefit the graft survival by repressing a set of inflammation/immunity related genes, and by modulating atherosclerosis especially through the blockage of TGFβ pathway. Heart graft function might also be improved by Rosi treatment through the protection of cardiac structure. Endothelial cells provide a barrier between the host's circulating blood and the perivascular tissues of the graft. Endothelial cell activation upon injury featuring enhanced expression of adhesion molecules, major histocompatibility (MHC) molecules and chemokines, facilitates leukocyte infiltration and promotes graft rejection. To determine whether Rosi can inhibit endothelial cell activation, thereby prolonging graft survival, human umbilical vein endothelial cell (HUVEC) was used as an endothelial cell activation model. A newly developed pan-PPAR agonist (Pan) targeting three isotypes of PPARs was also tested in this study. Both Rosi and Pan showed inhibition of HUVEC activation, with Pan being more potent than Rosi. The inhibition mediated by Rosi and Pan, however, was not abrogated by the PPARγ antagonist GW9662. Furthermore, GW9662 alone inhibited HUVEC activation. Taken together, the present data indicate that both the PPARγ agonist Rosi and the pan-PPAR agonist Pan can inhibit HUVEC activation, which may partially contribute to the beneficial effect of Rosi in controlling graft rejection. Prolongation of graft survival by Rosi might also ascribe to the regulation of a set of genes, including inflammation/immunity related genes, atherosclerosis related genes and cardiac structure related genes. In conclusion, the present study suggests a potential role for PPAR agonists as ne


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Product Details
  • ISBN-13: 9781374673366
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 138
  • Weight: 336 gr
  • ISBN-10: 1374673366
  • Publisher Date: 27 Jan 2017
  • Binding: Paperback
  • Language: English
  • Spine Width: 8 mm
  • Width: 216 mm


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