A granulocyte inhibitory protein overexpressed in chronic renal disease regulates expression of interleukin 6 and interleukin 8.
收藏PubMed Central1994-01-04 更新2026-05-16 收录
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https://pmc.ncbi.nlm.nih.gov/articles/PMC42935/
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Growing evidence suggests that cytokine expression is influenced by locally produced mediators, thus modifying the pluripotential effects of cytokines toward a tissue-specific inflammatory reaction. The granulocyte inhibitory protein (GIP), a 23-kDa protein found to be significantly overexpressed in patients with chronic renal failure, increases autocrine transcription and expression of interleukin (IL) 6 and IL-8 in human mesangial cells. Moreover, GIP alone induced the transcription of c-jun mRNA; however, in combination with IL-6, it stimulated de novo synthesis of DNA and the transcription of both c-jun and c-fos genes. The data suggest that the overall effect of GIP results in the modulation of the glomerular response to injury and contributes to the progression of glomerulosclerosis. IMAGES:
提供机构:
National Academy of Sciences
创建时间:
1994-01-04



