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Interstitial fibrosis in the renal inner medulla in humans is associated with up‐regulation of miR‐382 and down‐regulation of kallikrein 5
Author(s) -
Kriegel Alison J,
Mladinov Domagoj,
Kelly Holly,
Langenstroer Peter,
See William,
Liang Mingyu
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.663.12
Subject(s) - kallikrein , medulla , renal medulla , fibrosis , endocrinology , medicine , chemistry , kidney , biochemistry , enzyme
MicroRNAs are important post transcriptional regulators of gene expression. Our lab has identified microRNA miR‐382 as a facilitating regulator of interstitial fibrosis in the renal medulla of mice and in cultured human kidney cells and determined that this regulation may be mediated by a suppression of kallikrein 5 (KLK5). KLK5 is a (chymo)trypsin like peptidase capable of degrading extracellular matrix proteins. The goal of this study was to determine if there is an association between the levels of interstitial fibrosis, miR‐382 and KLK5 in human kidneys. Non‐tumor kidney tissue samples were obtained from patients who underwent partial or complete nephrectomy to remove renal tumors (n=6). The renal cortex, outer medulla and inner medulla were evaluated for fibrosis, miR‐382 expression and KLK5 expression using trichrome staining, in situ hybridization and immunohistochemistry, respectively. In the inner medulla miR‐382 expression correlated positively with fibrosis (R 2 =0.75) and negatively with KLK5 expression (R 2 =0.52). A positive correlation between miR‐382 and interstitial fibrosis was also detected in the outer medulla. These data indicate that alterations in miR‐382 are consistent with contribution to interstitial fibrosis via KLK5 in the inner medulla of human kidney.