Research on the mechanism of endothelin inflammatory effects on human mesangial cells

Yipu Chen, Yijuan Sun, Jingmei Lin, Anyu Zhou, Haiyan Wang

Research output: Contribution to journalArticle

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Abstract

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 (10-7mol/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.

Original languageEnglish (US)
Pages (from-to)530-534
Number of pages5
JournalChinese Medical Journal
Volume110
Issue number7
StatePublished - 1997
Externally publishedYes

Fingerprint

Mesangial Cells
Endothelins
Endothelin-1
Vascular Cell Adhesion Molecule-1
Intercellular Adhesion Molecule-1
Research
RNA
Up-Regulation
Tumor Necrosis Factor-alpha
Interleukin-1
Immunosorbents
Proteins
Thymocytes
Glomerulonephritis
Mitogens
Northern Blotting
Radioimmunoassay

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Research on the mechanism of endothelin inflammatory effects on human mesangial cells. / Chen, Yipu; Sun, Yijuan; Lin, Jingmei; Zhou, Anyu; Wang, Haiyan.

In: Chinese Medical Journal, Vol. 110, No. 7, 1997, p. 530-534.

Research output: Contribution to journalArticle

Chen, Yipu ; Sun, Yijuan ; Lin, Jingmei ; Zhou, Anyu ; Wang, Haiyan. / Research on the mechanism of endothelin inflammatory effects on human mesangial cells. In: Chinese Medical Journal. 1997 ; Vol. 110, No. 7. pp. 530-534.
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title = "Research on the mechanism of endothelin inflammatory effects on human mesangial cells",
abstract = "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 (10-7mol/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.",
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T1 - Research on the mechanism of endothelin inflammatory effects on human mesangial cells

AU - Chen, Yipu

AU - Sun, Yijuan

AU - Lin, Jingmei

AU - Zhou, Anyu

AU - Wang, Haiyan

PY - 1997

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N2 - 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 (10-7mol/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.

AB - 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 (10-7mol/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.

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