Related Experiment Video
Updated: Aug 12, 2026
Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Cytokine-induced expression of leukemia inhibitory factor in renal mesangial cells
A Hartner1, R B Sterzel, N Reindl
1Medizinische Klinik IV, Universitaet Erlangen-Nuernberg, Germany.
Insights
Glomerular mesangial cells produce and respond to Leukemia inhibitory factor (LIF), a cytokine that may play a role in kidney function. LIF expression is induced by inflammatory signals but is not mitogenic for these cells.
Area of Science:
- Nephrology
- Cell Biology
- Immunology
Background:
- Leukemia inhibitory factor (LIF) is a cytokine with roles in inflammation.
- Its involvement in mesangial cell regulation is not well understood.
Purpose of the Study:
- To investigate LIF expression in rat and human mesangial cells.
- To determine the response of mesangial cells to exogenous LIF.
Main Methods:
- Primary cultures of rat and human mesangial cells.
- Northern blot analysis for mRNA expression.
- ELISA for protein detection.
- Stimulation with various cytokines, growth factors, and LPS.
Main Results:
- Mesangial cells constitutively express low LIF mRNA levels.
- LIF mRNA expression is strongly induced by IL-1β, TNFα, PDGF, and LPS.
- Dexamethasone inhibits LIF induction; TGF-β shows synergy with IL-1β.
- LIF protein is detected in stimulated human mesangial cells.
- LIF induces immediate early genes (c-fos, jun-B, Egr-1) but is not mitogenic.
Conclusions:
- Glomerular mesangial cells produce and respond to LIF.
- LIF may have autocrine functions in the glomerulus.
- Further research is needed to clarify LIF's physiological and pathophysiological roles.
Abstract:
Leukemia inhibitory factor (LIF) is a pleiotropic cytokine, which shares many characteristics with interleukin-6 (IL-6). Recent observations indicate a role for LIF in inflammatory processes. To examine the potential involvement of LIF in the regulation of mesangial cell behavior, we studied LIF expression in early primary cultures of rat and human mesangial cells, as well as the response of mesangial cells to exogenous LIF. Growing or growth-arrested rat mesangial cells constitutively expressed very low levels of LIF mRNA, barely detectable by Northern blot analysis. Strong induction of LIF mRNA expression was caused by cytokines, such as interleukin-1 beta (5 ng/ml), tumor necrosis factor alpha (100 ng/ml) and PDGF (100 ng/ml), as well as LPS (200 ng/ml). The induction was transient with a peak after three to five hours. Dexamethasone (0.1 microM) almost completely inhibited the induction of LIF. Weak induction of LIF mRNA was observed after stimulation with basic fibroblast growth factor, endothelin and transforming growth factor beta. In combination with IL-1 beta, TGF beta showed synergistic effects on LIF induction. LIF itself or IL-6 had no effect on LIF mRNA expression. A similar induction pattern was observed for the expression of IL-6 mRNA. LIF protein was detected by specific ELISA in the supernatants of human mesangial cells stimulated by LPS or IL-1 beta. In addition, we found that mesangial cells not only express LIF but they are also target cells for LIF. Recombinant LIF effectively induced transient expression of the immediate early genes, c-fos, jun-B and Egr-1 in rat mesangial cells, with a maximum at 30 to 60 minutes. LIF was not mitogenic for mesangial cells. Our findings indicate that glomerular mesangial cells produce and react to LIF. As a cytokine with autocrine potential, LIF may play a physiological and/or pathophysiological role in the glomerulus, the exact nature and relevance of which remain to be explored.
