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MicroRNA expression regulates cardiac fibrosis in Uremic Cardiomyopathy
Author(s) -
Drummond Christopher Anson,
Haller Steven,
Shapiro Joseph I,
Tian Jiang
Publication year - 2013
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.27.1_supplement.726.4
Subject(s) - fibrosis , microrna , cardiac fibrosis , medicine , endocrinology , cardiomyopathy , phenotype , muscle hypertrophy , biology , cancer research , heart failure , gene , biochemistry
In rats, uremic cardiomyopathy via 5/6 th partial nephrectomy (PNx) displays cardiac hypertrophy and fibrosis. Studies in our lab have revealed a crucial role for Na/K‐ATPase signaling as mediated through cardiotonic steroids in the development of this phenotype. Molecular regulators of this disease process are poorly understood; as such we found reports linking fibrotic diseases with micro RNA (miRNA) expression. Reports indicate that miR‐29b directly targets collagen mRNA and that expression of miR‐29b is decreased in fibrotic tissues. We examined miR‐29b levels in rat hearts from the following groups: sham controls, PNx and MBG‐infused animals. The qPCR data showed that PNx and MBG‐infusion, significantly decreased miR‐29b by 3.18‐ and 2.33‐fold, respectively. In point of fact, collagen expression increased significantly in both PNx (7.7‐fold) and MBG‐infused (6.4‐fold) animals versus sham controls. Additional array based studies revealed that in PNx and MBG‐infused animals 17 miRNAs were dysregulated in both groups these miRNAs include: 29b, 124, 144, 122, 32, 141,196b, 96, 423, 210, 375, 182, 196a, and 324–5p. These miRNAs were found to be associated heavily with the development of fibrosis and apoptosis. We conclude that dysregulation of miRNA expression is mechanistically linked with the development of the phenotype observed in uremic cardiomyopathy. Supported by NIH HL‐105649