Limitations of commonly used internal controls for real-time RT-PCR analysis of renal epithelial-mesenchymal cell transition

Nephron Exp Nephrol. 2006;102(3-4):e113-22. doi: 10.1159/000090070. Epub 2005 Dec 7.

Abstract

Background/aims: Progressive renal fibrotic disease is accompanied by the massive accumulation of myofibroblasts as defined by alpha smooth muscle actin (alphaSMA) expression. We quantitated gene expression using real-time RT-PCR analysis during conversion of primary cultured human renal tubular cells (RTC) to myofibroblasts after treatment with transforming growth factor-beta1 (TGF-beta1). We report herein the limitations of commonly used reference genes for mRNA quantitation.

Methods: We determined the expression of alphaSMA and megakaryoblastic leukemia-1 (MKL1), a transcriptional regulator of alphaSMA, by quantitative real-time PCR using three common internal controls, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), cyclophilin A and 18S rRNA.

Results: Expression of GAPDH mRNA and cyclophilin A mRNA, and to a lesser extent, 18S rRNA levels varied over time in culture and with exposure to TGF-beta1. Thus, depending on which reference gene was used, TGF-beta1 appeared to have different effects on expression of MKL1 and alphaSMA.

Conclusions: RTC converting to myofibroblasts in primary culture is a valuable system to study renal fibrosis in humans. However, variability in expression of reference genes with TGF-beta1 treatment illustrates the need to validate mRNA quantitation with multiple reference genes to provide accurate interpretation of fibrosis studies in the absence of a universal internal standard for mRNA expression.

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Cell Differentiation
  • Cells, Cultured
  • Computer Systems* / standards
  • Cyclophilin A / genetics
  • Fibroblasts / pathology*
  • Fibrosis
  • Gene Expression
  • Glyceraldehyde-3-Phosphate Dehydrogenases / genetics
  • Humans
  • Kidney Tubules / drug effects
  • Kidney Tubules / metabolism*
  • Kidney Tubules / pathology*
  • MAP Kinase Kinase Kinases / genetics
  • Muscle, Smooth / metabolism
  • Myocytes, Smooth Muscle / pathology*
  • Quality Control*
  • RNA, Ribosomal, 18S / genetics
  • Reverse Transcriptase Polymerase Chain Reaction* / standards
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta1

Substances

  • Actins
  • RNA, Ribosomal, 18S
  • TGFB1 protein, human
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Glyceraldehyde-3-Phosphate Dehydrogenases
  • MAP Kinase Kinase Kinases
  • MAP3K9 protein, human
  • Cyclophilin A