Transforming growth factor-beta1 and tumor growth factor-beta-inducible gene-H3 in nonrenal transplant cyclosporine nephropathy

Transplantation. 2001 Dec 15;72(11):1826-9. doi: 10.1097/00007890-200112150-00019.

Abstract

Cyclosporine nephropathy (CyAN) is a major limiting factor in the otherwise successful widespread use of cyclosporine in solid organ transplant. Transforming growth factor-beta1 (TGF-beta1) has been implicated as an important fibrogenic cytokine in the development of this disease. TGF-beta-inducible gene-H3 (beta(ig)-H3) is a TGF-beta1- induced gene product, which acts as a marker for biologically active TGF-beta1. This study reports TGF-beta1 gene expression and beta(ig)-H3 tissue distribution in non-renal allograft CyAN. Renal tissue from nine patients who had developed CyAN after successful heart or heart-lung transplantation and from four kidneys removed for tumour were analyzed for TGF-beta1 gene expression beta(ig)-H3 protein with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry, respectively. TGF-beta1 gene expression was increased in CyAN compared to nephrectomy (P<0.0001). Beta(ig)-H3 protein expression was identified in distal convoluted tubular epithelium and parietal glomerular epithelium in CyAN, and not in nephrectomy samples. Expression of TGF-beta1 mRNA was significantly higher in renal tissue from patients not receiving angiotensin converting enzyme inhibitor (ACEI) therapy for hypertension (P<0.05). These findings support the hypothesis that TGF-beta1 is an important cytokine in the development of CyAN, independent of its role in chronic rejection in renal allografts.

MeSH terms

  • Adult
  • Cyclosporine / adverse effects*
  • Extracellular Matrix Proteins*
  • Heart Transplantation*
  • Heart-Lung Transplantation*
  • Humans
  • Immunosuppressive Agents / adverse effects*
  • Kidney / metabolism
  • Kidney Diseases / chemically induced*
  • Kidney Diseases / metabolism*
  • Kidney Tubules, Distal / metabolism
  • Middle Aged
  • Neoplasm Proteins / metabolism*
  • RNA, Messenger / metabolism
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism*
  • Transforming Growth Factor beta1

Substances

  • Extracellular Matrix Proteins
  • Immunosuppressive Agents
  • Neoplasm Proteins
  • RNA, Messenger
  • TGFB1 protein, human
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • betaIG-H3 protein
  • Cyclosporine