摘要
Objective To investigate the mechanism of endothelin (ET) inflammatory effects on human mesangial cells (HMC). Methods The following experiments were performed on cultured HMC after ET 1 stimulation: (1) the expression of tumor necrosis factor α (TNFα), interleukin 1β (IL 1β), intercellular adhesion molecule 1 (ICAM 1), vascular cell adhesion molecule 1 (VCAM 1) and endothelin 1 (ET 1) itself messenger ribonucleic acid (mRNA) was determined by Northern Blot analysis; (2) the TNFα concentration was tested with radioimmunoassay; the IL 1 activity was assayed by the enhancement of thymocyte proliferation in response to mitogen; the surface expression of ICAM 1 and VCAM 1 was measured with cell emzyme linked immunoadsorbent assay (ELISA) analysis. Results ET 1 (10 -7 mol/L) induced the following changes on HMC: (1) up regulation of the expression of TNFα mRNA and protein; (2) up regulation of the expression of ICAM 1 and VCAM 1 mRNA and protein; (3) up regulation of the expression of ET 1 itself mRNA. However, the expression of IL 1 mRNA and protein was not changed. Conclusions ET 1 can stimulate HMC to produce TNFα, ICAM 1 and VCAM 1, and there by induce inflammatory effects. ET 1 can also stimulate HMC to up regulate the expression of ET 1 itself, so as to amplify inflammatory effects. So, ET 1 is actually an inflammatory mediator and may play an important role in the pathogenesis of glomerulonephritis.
Objective To investigate the mechanism of endothelin (ET) inflammatory effects on human mesangial cells (HMC). Methods The following experiments were performed on cultured HMC after ET 1 stimulation: (1) the expression of tumor necrosis factor α (TNFα), interleukin 1β (IL 1β), intercellular adhesion molecule 1 (ICAM 1), vascular cell adhesion molecule 1 (VCAM 1) and endothelin 1 (ET 1) itself messenger ribonucleic acid (mRNA) was determined by Northern Blot analysis; (2) the TNFα concentration was tested with radioimmunoassay; the IL 1 activity was assayed by the enhancement of thymocyte proliferation in response to mitogen; the surface expression of ICAM 1 and VCAM 1 was measured with cell emzyme linked immunoadsorbent assay (ELISA) analysis. Results ET 1 (10 -7 mol/L) induced the following changes on HMC: (1) up regulation of the expression of TNFα mRNA and protein; (2) up regulation of the expression of ICAM 1 and VCAM 1 mRNA and protein; (3) up regulation of the expression of ET 1 itself mRNA. However, the expression of IL 1 mRNA and protein was not changed. Conclusions ET 1 can stimulate HMC to produce TNFα, ICAM 1 and VCAM 1, and there by induce inflammatory effects. ET 1 can also stimulate HMC to up regulate the expression of ET 1 itself, so as to amplify inflammatory effects. So, ET 1 is actually an inflammatory mediator and may play an important role in the pathogenesis of glomerulonephritis.
