Objective: To investigate whether hPTH1-34 regulate the synthesis of fibronectin (FN) from cultured rat mesangial cells and its possible mechanism. Methods: (1) MCs seeded at a density of 1 × 104 per well in 24-w...Objective: To investigate whether hPTH1-34 regulate the synthesis of fibronectin (FN) from cultured rat mesangial cells and its possible mechanism. Methods: (1) MCs seeded at a density of 1 × 104 per well in 24-well plates were treated with medium containing various concentrations of hPTH1-34(10-12 mol/l -10-8 mol/l) for 6 h, 12 h, 24 h and 48 h, control cells were treated with vehicle only. The FN levels (in the supernatant) were measured by ELISA assay. (2) MCs were co-cultured with 10 ng/l of anti-TGF-β antibody and various concentrations of hPTH1-34(10-12 mol/l - 10-8 mol/l ). Forty-eight hours later, FN were tested by ELISA. (4) MCs were co-cultured with 10 ng/l of anti-TGF-β antibody and 10-8 mol/l hPTH1-34 for 6 h, 12 h, 24 h and 48 h and then FN were tested. Results: (1) hPTH1-34 stimulated FN synthesis in a dose-and time-dependent way with a peak at 10-8 mol/l (P<0. 01). (2) Anti-TGF-β antibody inhibited the stimulation effect of hPTH1-34, on synthesis of FN in cultured rat mesangial cells (P<0. 05). Conclusion: hPTH1-34 up-regulates FN synthesis in cultured rat mesangial cells via TGF-β, suggesting that PTH may play an important role in deteriorating the residual renal function at the early stage of chronic renal disease.展开更多
文摘众所周知,几乎所有终末期肾功能衰竭患者都伴随着代谢性骨病.此类骨病,在二十世纪三十年代的个案报告中被称为"肾性佝偻病"(renal rick-ets);而十年后,经过两位中国内分泌专家刘士豪、朱宪彝的系统研究,则将其称为"肾性骨营养不良"(renal osteodystrophy)(Medicine,1943;2:103-161),并一直沿用至今,目前一般简称"肾性骨病"(renal bone disease).
文摘Objective: To investigate whether hPTH1-34 regulate the synthesis of fibronectin (FN) from cultured rat mesangial cells and its possible mechanism. Methods: (1) MCs seeded at a density of 1 × 104 per well in 24-well plates were treated with medium containing various concentrations of hPTH1-34(10-12 mol/l -10-8 mol/l) for 6 h, 12 h, 24 h and 48 h, control cells were treated with vehicle only. The FN levels (in the supernatant) were measured by ELISA assay. (2) MCs were co-cultured with 10 ng/l of anti-TGF-β antibody and various concentrations of hPTH1-34(10-12 mol/l - 10-8 mol/l ). Forty-eight hours later, FN were tested by ELISA. (4) MCs were co-cultured with 10 ng/l of anti-TGF-β antibody and 10-8 mol/l hPTH1-34 for 6 h, 12 h, 24 h and 48 h and then FN were tested. Results: (1) hPTH1-34 stimulated FN synthesis in a dose-and time-dependent way with a peak at 10-8 mol/l (P<0. 01). (2) Anti-TGF-β antibody inhibited the stimulation effect of hPTH1-34, on synthesis of FN in cultured rat mesangial cells (P<0. 05). Conclusion: hPTH1-34 up-regulates FN synthesis in cultured rat mesangial cells via TGF-β, suggesting that PTH may play an important role in deteriorating the residual renal function at the early stage of chronic renal disease.
