Nephrectomy enhances interleukin 6 secretion by interleukin 1-stimulated mesangial cells in vitro.
Joshua Weissgarten, Ahuva Golik, M. Cohn, Dishi, Nir Cohen, Sylvia Berman, David Modai, Zhan Averbukh
Abstract
Joshua Weissgarten, Ahuva Golik, M. Cohn, Dishi, Nir Cohen, Sylvia Berman, David Modai, Zhan Averbukh
Abstract
BACKGROUND: Kidney mesangial cells are capable of producing and responding to interleukin 6 (IL-6) . In experimental glomerulonephritis mesangial cell proliferation correlates with increased IL-6 production. To investigate the involvement of IL-6 in post-nephrectomy compensatory hypertrophy, we studied the capacity of mesangial cells from single remaining kidneys to secrete IL-6 in culture. METHODS: Mesangial cells were obtained from uni-nephrectomized or sham-nephrectomized Charles River rats. Cell cultures were maintained for 8 days in DMEM/FI2HAM medium supplemented with IL-1 of interferon (IFN). IL6 production was measured using an IL-6-dependent B9 human hybridoma cell line. RESULTS: IL-6 production by mesangial cells from normal kidneys was significantly enhanced by IL-1, compared to unstimulated cells (p<0.01), and the increase was significantly greater in mesangial cells from a single remaining kidney (p<0.01). All cultures grown in control medium or with addition of IFN produced similar amounts of IL-6. CONCLUSION: Mesangial cells from single remaining kidneys in culture maintain an exaggerated capacity to produce IL-6 in response to IL-1. IL-6 was reported to enhance or inhibit mesangial cell proliferation in vitro. We suggest that the local over production of IL-6 by a single remaining kidney may play a role in regulating a sequence of physiological events in compensatory renal growth, initially stimulating mesangial cell proliferation and later blunting the process.
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BACKGROUND: Kidney mesangial cells are capable of producing and responding to interleukin 6 (IL-6) . In experimental glomerulonephritis mesangial cell proliferation correlates with increased IL-6 production. To investigate the involvement of IL-6 in post-nephrectomy compensatory hypertrophy, we studied the capacity of mesangial cells from single remaining kidneys to secrete IL-6 in culture. METHODS: Mesangial cells were obtained from uni-nephrectomized or sham-nephrectomized Charles River rats. Cell cultures were maintained for 8 days in DMEM/FI2HAM medium supplemented with IL-1 of interferon (IFN). IL6 production was measured using an IL-6-dependent B9 human hybridoma cell line. RESULTS: IL-6 production by mesangial cells from normal kidneys was significantly enhanced by IL-1, compared to unstimulated cells (p<0.01), and the increase was significantly greater in mesangial cells from a single remaining kidney (p<0.01). All cultures grown in control medium or with addition of IFN produced similar amounts of IL-6. CONCLUSION: Mesangial cells from single remaining kidneys in culture maintain an exaggerated capacity to produce IL-6 in response to IL-1. IL-6 was reported to enhance or inhibit mesangial cell proliferation in vitro. We suggest that the local over production of IL-6 by a single remaining kidney may play a role in regulating a sequence of physiological events in compensatory renal growth, initially stimulating mesangial cell proliferation and later blunting the process.
Key concepts: Mesangial cell, Medicine, Internal medicine, Endocrinology, Mesangial proliferative glomerulonephritis, Secretion, Cytokine, Cell growth