Expression of transgelin in human glomerulonephritis of various etiology

Nephron Clin Pract. 2011;119(1):c74-82. doi: 10.1159/000324655. Epub 2011 Jun 15.

Abstract

Background/aims: Activation of myofibroblasts occurs during kidney injury. Genomic and proteomic studies suggest that transgelin represents a protein that may be involved in renal injury. The purpose of this study was to estimate transgelin expression in the renal tissue of patients with glomerulonephritis.

Methods: Transgelin was identified in biopsy sections of 67 patients by immunohistochemistry and immunofluorescence. Its distribution was compared to that of α-smooth muscle actin (α-SMA), a marker of myofibroblast activation in the kidney.

Results: Transgelin and α-SMA expression was identified within glomeruli and interstitium. In patients with IgA nephropathy and focal segmental glomerulosclerosis, glomerular expression of transgelin was higher than that of α-SMA. The extent of transgelin immunostaining was related to mesangial proliferation (p = 0.034), glomerular sclerosis (p = 0.035), interstitial fibrosis (p = 0.047) and to the clinical course (p = 0.009). Colocalization studies showed that in some areas of kidney tissue both proteins were expressed with comparable intensity, whereas in other areas expression of either transgelin or α-SMA was predominant.

Conclusion: Strong transgelin expression was observed in renal tissue of patients with glomerulonephritis. The observed differences in the pattern of transgelin and α-SMA expression suggest that either different subpopulations of myofibroblasts exist, or that these proteins are activated at different stages of renal injury/scarring.

Publication types

  • Comparative Study

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Adult
  • Aged
  • Biomarkers / metabolism
  • Female
  • Follow-Up Studies
  • Gene Expression Regulation*
  • Glomerulonephritis / etiology*
  • Glomerulonephritis / genetics
  • Glomerulonephritis / metabolism*
  • Humans
  • Kidney / cytology
  • Kidney / metabolism
  • Kidney / pathology
  • Male
  • Microfilament Proteins / biosynthesis*
  • Microfilament Proteins / genetics
  • Middle Aged
  • Muscle Proteins / biosynthesis*
  • Muscle Proteins / genetics
  • Myofibroblasts / metabolism
  • Tissue Distribution / genetics

Substances

  • ACTA2 protein, human
  • Actins
  • Biomarkers
  • Microfilament Proteins
  • Muscle Proteins
  • transgelin