Nephrectomy enhances interleukin 6 secretion by interleukin 1-stimulated mesangial cells in vitro

J Weissgarten1, A Golik, M Cohn

  • 1Nephrology Division, Assaf Harofeh Medical Center, Sackler School of Medicine, Tel-Aviv University, Zerifin, Israel.

Journal of Nephrology
|August 14, 1998
PubMed

Insights

Kidney mesangial cells in remaining kidneys show increased interleukin-6 (IL-6) production after nephrectomy. This heightened IL-6 may regulate compensatory renal growth by initially stimulating and later inhibiting cell proliferation.

Area of Science:

  • Nephrology
  • Cell Biology
  • Immunology

Background:

  • Kidney mesangial cells produce and respond to interleukin-6 (IL-6).
  • Increased IL-6 production correlates with mesangial cell proliferation in experimental glomerulonephritis.
  • The role of IL-6 in compensatory renal hypertrophy post-nephrectomy requires investigation.

Purpose of the Study:

  • To investigate the involvement of IL-6 in post-nephrectomy compensatory hypertrophy.
  • To assess the capacity of mesangial cells from single remaining kidneys to secrete IL-6 in culture.

Main Methods:

  • Mesangial cells were isolated from uni-nephrectomized or sham-nephrectomized rats.
  • Cell cultures were maintained and stimulated with IL-1 or interferon (IFN).
  • IL-6 production was quantified using an IL-6-dependent hybridoma cell line.

Main Results:

  • IL-1 significantly enhanced IL-6 production in mesangial cells from normal kidneys.
  • Mesangial cells from single remaining kidneys exhibited a significantly greater IL-1-induced IL-6 production compared to normal kidneys.
  • Interferon (IFN) did not affect IL-6 production.

Conclusions:

  • Mesangial cells from single remaining kidneys demonstrate an exaggerated IL-6 production capacity in response to IL-1.
  • This localized overproduction of IL-6 may regulate compensatory renal growth.
  • IL-6 might initially stimulate and subsequently attenuate mesangial cell proliferation during renal hypertrophy.
Abstract