Open AccessHigh glucose induces macrophage inflammatory protein-3 in renal proximal tubule cells via a transforming growth factor- 1 dependent mechanism
Author(s) -
Weiwei Qi,
Xinming Chen,
Y. Zhang,
John Holian,
Ellein Mreich,
Richard E. Gilbert,
Darren J. Kelly,
Carol A. Pollock
Publication year - 2007
Publication title -
nephrology dialysis transplantation
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfm365
Subject(s) - medicine , chemokine , inflammation , transforming growth factor , pathogenesis , diabetic nephropathy , fibrosis , nephropathy , macrophage , kidney , growth factor , diabetes mellitus , transforming growth factor beta , endocrinology , immunology , receptor , biology , biochemistry , in vitro
Hyperglycaemia is a causative factor in the pathogenesis of diabetic nephropathy, known to induce chemokines in the kidney. Macrophage inflammatory protein-3 alpha (MIP-3 alpha) is a CC chemokine that has been reported to attract memory T lymphocytes. Our previous microarray study showed significant increased level of MIP-3 alpha in high glucose-induced transcriptional profile in renal proximal tubule cells. Transforming growth factor-beta1 (TGF-beta1) is a key regulator in inflammation and fibrosis in diabetes mellitus setting.
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