Unknown,Transcriptomics,Genomics,Proteomics

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A master cistromic circuit governing hepatic fibrogenesis [expression array]


ABSTRACT: Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Expression profiling was used to explore the potential impact of VDR signaling in TGF?1 and TGF?1+1,25(OH)2D3-treated primary rat HSCs. Notably, 1,25(OH)2D3 treatment attenuated the culture-induced activation of HSCs, such that the transcriptome of treated cells closely resembled that of freshly isolated quiescent cells (Figure 2A), and co-treatment of 1,25(OH)2D3 together with TGF? resulted in considerable repression of a large set of TGF? induced genes. We also demonstrated that in primary mouse HSCs, calcipotriol potently repressed fibrotic gene expression, suggesting that the anti-TGF? properties of VDR agonists are likely conserved across mammalian species. Total RNA from primary rat HSCs were isolated and treated 1,25(OH)2D3 (100nM) for 24 hours to determine how Vitamin D ligands can impact the activated stellate cell state.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Ruth Yu 

PROVIDER: E-GEOD-41579 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


Liver fibrosis is a reversible wound-healing response involving TGFβ1/SMAD activation of hepatic stellate cells (HSCs). It results from excessive deposition of extracellular matrix components and can lead to impairment of liver function. Here, we show that vitamin D receptor (VDR) ligands inhibit HSC activation by TGFβ1 and abrogate liver fibrosis, whereas Vdr knockout mice spontaneously develop hepatic fibrosis. Mechanistically, we show that TGFβ1 signaling causes a redistribution of genome-wid  ...[more]

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