Weissgarten J, Golik A, Cohn M, Dishi V, Cohen N, Berman S, Modai D, Averbukh Z
Nephrology Division, Assaf Harofeh Medical Center, Sackler School of Medicine, Tel-Aviv University, Zerifin, Israel.
J Nephrol. 1998 Jul-Aug;11(4):199-202.
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.
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.
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.
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.
肾系膜细胞能够产生并对白细胞介素6(IL-6)作出反应。在实验性肾小球肾炎中,系膜细胞增殖与IL-6产生增加相关。为了研究IL-6在肾切除术后代偿性肥大中的作用,我们研究了来自单个留存肾脏的系膜细胞在培养中分泌IL-6的能力。
系膜细胞取自单侧肾切除或假手术切除的查尔斯河大鼠。细胞培养物在补充有干扰素(IFN)的IL-1的DMEM/F12HAM培养基中维持8天。使用依赖IL-6的B9人杂交瘤细胞系测量IL-6的产生。
与未刺激的细胞相比,IL-1显著增强了正常肾脏系膜细胞的IL-6产生(p<0.01),并且来自单个留存肾脏的系膜细胞中的增加显著更大(p<0.01)。在对照培养基中或添加IFN培养的所有细胞产生相似量的IL-6。
培养中来自单个留存肾脏的系膜细胞对IL-1刺激保持过度产生IL-6的能力。据报道,IL-6在体外可增强或抑制系膜细胞增殖。我们认为单个留存肾脏局部过度产生IL-6可能在调节代偿性肾脏生长中的一系列生理事件中起作用,最初刺激系膜细胞增殖,随后使该过程减弱。