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Gene expression profile in human mesangial cells stimulated with aldosterone
Author(s) -
Romero Damian G
Publication year - 2009
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.23.1_supplement.801.3
Subject(s) - mineralocorticoid receptor , downregulation and upregulation , microbiology and biotechnology , aldosterone , biology , signal transduction , notch signaling pathway , intracellular , mapk/erk pathway , cancer research , endocrinology , gene , genetics
Primary hyperaldosteronism is the most common cause of secondary hypertension and is associated with renal injury. Mesangial cells (MC) regulate glomeruli structure and are involved in multiple renal diseases. It has been previously reported that MC express the mineralocorticoid receptor and aldosterone (ALDO) regulates cell proliferation and oxidative stress among many other physio‐ and pathophysiological actions in MC. However, the molecular mechanisms that trigger the onset and progression of MC‐mediated renal injury by excess ALDO are not clear. We studied whole genome gene expression in human MC (HMC) to analyze which are the intracellular pathways involved in ALDO‐mediated glomeruli injury. HMC were treated with ALDO (10 nM) for 3 or 24 h and their transcriptome analyzed with Illumina BeadChips. Significantly regulated genes were used to analyze the early and late intracellular pathways modulated by ALDO. ALDO treatment for 3 h upregulated glycosphingolipid biosynthesis, and the Notch and Hedgehog signaling pathways, while significantly downregulated genes involved in cell cycle and division. ALDO treatment for 24 h upregulated ubiquitin‐mediated proteolysis and MAPK signaling pathways, and several transcription factors (PML, ELK4, SP6, ZNF323, ZXDC, MIZF). This study highlights new early and late intracellular pathways triggered by ALDO in HMC that may be involved in ALDO‐mediated renal injury