RGD Reference Report - The effect of acute rejection and cyclosporin A-treatment on induction of platelet-derived growth factor and its receptors during the development of chronic rat renal allograft rejection. - Rat Genome Database

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The effect of acute rejection and cyclosporin A-treatment on induction of platelet-derived growth factor and its receptors during the development of chronic rat renal allograft rejection.

Authors: Savikko, J  Kallio, EA  Taskinen, E  Von Willebrand, E 
Citation: Savikko J, etal., Transplantation. 2002 Feb 27;73(4):506-11.
RGD ID: 11080974
Pubmed: PMID:11889420   (View Abstract at PubMed)

BACKGROUND: In the development of chronic kidney allograft rejection acute rejection (AR) is the single most important risk factor. Although Cyclosporin A (CsA) medication has decreased the incidence of AR, chronic rejection (CR) is still the major reason for late allograft loss. Platelet-derived growth factor (PDGF) is a major mitogen mediating mesenchymal cell proliferation in CR. We have investigated the impact of AR and different doses of CsA on the expression of PDGF ligands and receptors in the development of CR. METHODS: Kidney transplantations were performed from DA to WF rats and syngenic controls were done from DA to DA rats. Two groups of allografts were treated daily with CsA either at low dose (1.5 mg/kg) or high dose (5 mg/kg). Third group of allografts was treated with CsA 5 mg/kg/day for 1 week and then left untreated until the development of AR. AR episodes were treated with CsA 5 mg/kg/day. Grafts were harvested 3 months after transplantation for histology and immunohistochemistry (PDGF-AA, -BB and PDGFR-alpha, -beta). RESULTS: In syngenic grafts no histological signs of CR were seen and the expression of PDGF ligands and receptors remained almost nonexistent. AR episodes increased the chronic rejection changes. High-dose CsA-treatment ameliorated inflammation compared to low-dose CsA-treatment, although it failed to inhibit the development of chronic changes. More fibrosis was even seen in high-dose than in low-dose CsA-treated grafts. CR in each allograft group was associated with induction of all PDGF ligands and receptors (P<0.05 compared with syngenic controls) in interstitial inflammatory cells, capillary endothelium, and arterial smooth muscle cells. In the group with AR episodes the expression was further increased. CONCLUSIONS: Our results demonstrate that CsA treatment cannot inhibit the expression of PDGF ligands and receptors in the development of chronic kidney allograft rejection and that AR episodes induce even more PDGF and its receptors in the graft indicating a link between AR and subsequent development of CR.




Objects Annotated

Genes (Rattus norvegicus)
Pdgfa  (platelet derived growth factor subunit A)
Pdgfb  (platelet derived growth factor subunit B)
Pdgfra  (platelet derived growth factor receptor alpha)
Pdgfrb  (platelet derived growth factor receptor beta)

Genes (Mus musculus)
Pdgfa  (platelet derived growth factor, alpha)
Pdgfb  (platelet derived growth factor, B polypeptide)
Pdgfra  (platelet derived growth factor receptor, alpha polypeptide)
Pdgfrb  (platelet derived growth factor receptor, beta polypeptide)

Genes (Homo sapiens)
PDGFA  (platelet derived growth factor subunit A)
PDGFB  (platelet derived growth factor subunit B)
PDGFRA  (platelet derived growth factor receptor alpha)
PDGFRB  (platelet derived growth factor receptor beta)


Additional Information