Figure 3 LncRNAs in kidney disease

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Figure 3 LncRNAs in kidney disease Figure 3 | LncRNAs in kidney disease. LncRNAs modulate several physiological and pathogenic processes in the kidney. Embryonic kidney development: dysregulation of Mest and H19 expression in the embryonic kidneys of mice with hyperglycaemic mothers leads to impaired epithelial–mesenchymal interactions and epigenetic changes, which might affect disease susceptibility in adult life. Hypertension: altered expression of lncRNAs correlates with changes in the expression of target genes, including ankyrin repeat and SOCS box 3 (Asb3), cation transport regulator homologue 2 (Chac2), peroxisomal membrane protein 11B (Pex11b), and trans-acting transcription factor 5 (Sp5). Membranous nephropathy: Xist and NEAT1 levels are increased in mice with membranous nephropathy; reduced H3K27me3 occupancy was found at the Xist promoter. Mesangial glomerulonephritis: an altered lncRNA expression profile has been reported. Diabetic nephropathy: high glucose levels increase the levels of PVT1, fibronectin 1 (FN1), collagen type IV α1 (COL4A1), transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor-1 (PAI-1) in mesangial cells and induce the expression of MALAT1, serum amyloid antigen 3 (SAA3), TNF and IL-6 in endothelial cells. Acute kidney injury: plasma levels of TapSAKI, possibly derived from tubular epithelial cells, are increased in patients with acute kidney injury and predict survival. Inflammation and fibrosis: silencing of Arid2-IR in tubular epithelial cells reduces inflammation by altering IL-1β and NF-κB-mediated inflammatory pathways. The levels of the Smad3-dependent lncRNAs np_5318 and np_17856 were increased in murine models of unilateral ureteral obstruction and anti-glomerular basement membrane glomerulonephritis and associated with progressive renal inflammation and fibrosis. Renal cell carcinoma: a variety of lncRNAs are deregulated in renal cell carcinoma. HOTAIR silencing results in reduced proliferative and invasive potential of cancer cells. CADM1-AS1 is downregulated in tissue samples of patients with clear cell renal cell carcinoma, which leads to increased expression of CADM and increased proliferation and cell migration, and reduced cell apoptosis. Acute renal allograft rejection: urinary RP11-354P17.15-001 is increased in patients with acute rejection, normalized with immunosuppressive anti-rejection therapy and predicts kidney function at 1 year after transplantation. Lorenzen, J. M. & Thum, T. (2016) Long noncoding RNAs in kidney and cardiovascular diseases Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.51