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High glucose down‐regulates miR‐29a to increase collagen IV production in HK‐2 cells
Author(s) -
Du Bin,
Ma Li-Ming,
Huang Mian-Bo,
Zhou Hui,
Huang Hui-Lin,
Shao Peng,
Chen Yue-Qin,
Qu Liang-Hu
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.12.053
Subject(s) - chemistry , downregulation and upregulation , microbiology and biotechnology , repressor , microrna , medicine , endocrinology , diabetic nephropathy , biochemistry , gene expression , biology , kidney , gene
Deposition of collagen IV in proximal tubule cells (PTCs) plays an important role during diabetic nephropathy, but the mechanism underlying excessive production of collagen IV remains poorly understood. In this study, we examined the miRNA profile of HK‐2 cells and found that high glucose/TGF‐β1 induced significant down‐regulation of miR‐29a. We then showed that miR‐29a negatively regulated collagen IV by directly targeting the 3′UTRs of col4a1 and col4a2 . These results suggest that miR‐29a acts as a repressor to fine‐tune collagen expression and that the reduction of miR‐29a caused by high glucose may increase the risk of excess collagen deposition in PTCs.