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Interferon-gamma induces macrophage migration inhibitory factor synthesis and secretion by tubular epithelial cells
Edwina K Rice1, David J Nikolic-Paterson, Prudence A Hill
1Departments of Nephrology and Medicine, Monash Medical Centre, Clayton, Victoria, Australia. edwina.rice@med.monash.edu.au
Abstract:
Macrophage migration inhibitory factor (MIF) promotes macrophage accumulation and leucocyte activation during inflammation. Macrophage migration inhibitory factor is upregulated in intrinsic renal cells in many types of kidney diseases, and has a pathogenic role in rat crescentic nephritis. However, little is known about the factors that regulate the production and secretion of MIF in kidney cells. In this study, we evaluated whether interferon-gamma (IFN-gamma), a cytokine implicated in the development of kidney disease and a potent inducer of MIF production in macrophages, could promote MIF synthesis and secretion from renal tubular epithelial cells. Northern blot analysis detected constitutive expression of MIF mRNA in rat tubular epithelial cells (NRK52E), which increased twofold after a 6-h stimulation with IFN-gamma. Macrophage migration inhibitory factor protein was found only in the cytoplasm of NRK52E cells. Following IFN-gamma stimulation, intracellular MIF in NRK52E cells was rapidly secreted with a maximal reduction of 50% after 20 min, which returned to normal levels after 2-4 h. Rapid secretion of MIF in response to IFN-gamma was also seen in rat mesangial cells. These findings indicate that IFN-gamma induces rapid secretion of MIF by tubular epithelial cells, and suggest that this may be an important mechanism leading to inflammatory cell accumulation and activation during kidney disease.
Insights
Interferon-gamma (IFN-gamma) rapidly induces the secretion of macrophage migration inhibitory factor (MIF) from kidney tubular epithelial cells. This suggests a key mechanism contributing to inflammation and cell accumulation in kidney diseases.
Area of Science:
- Immunology
- Nephrology
- Cell Biology
Background:
- Macrophage migration inhibitory factor (MIF) is implicated in kidney disease pathogenesis.
- Factors regulating MIF production in renal cells are largely unknown.
- Interferon-gamma (IFN-gamma) is a cytokine involved in kidney disease and a known MIF inducer in macrophages.
Purpose of the Study:
- To investigate if IFN-gamma stimulates MIF synthesis and secretion in renal tubular epithelial cells.
- To elucidate the role of IFN-gamma in regulating MIF in kidney cells.
Main Methods:
- Northern blot analysis to detect MIF mRNA expression in rat tubular epithelial cells (NRK52E).
- Assessment of intracellular and secreted MIF protein levels following IFN-gamma stimulation.
- Evaluation of MIF secretion kinetics in response to IFN-gamma.
Main Results:
- Constitutive MIF mRNA expression was observed in NRK52E cells.
- IFN-gamma stimulation led to a twofold increase in MIF mRNA after 6 hours.
- Intracellular MIF protein was rapidly secreted from NRK52E cells upon IFN-gamma exposure, with maximal reduction at 20 minutes.
- Similar rapid MIF secretion was observed in rat mesangial cells.
Conclusions:
- IFN-gamma induces rapid MIF secretion from renal tubular epithelial cells.
- This IFN-gamma-mediated MIF secretion may contribute to inflammatory cell accumulation and activation in kidney diseases.
- The study highlights a novel regulatory pathway for MIF in kidney cells relevant to disease progression.
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