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SRX9741001: GSM4990679: H3K27ac_Unstim_Rep2; Mus musculus; ChIP-Seq
1 ILLUMINA (NextSeq 500) run: 42.6M spots, 3.2G bases, 566.6Mb downloads

Submitted by: NCBI (GEO)
Study: A Transcriptional Switch Governs Fibroblast Activation in Heart Disease
show Abstracthide Abstract
In diseased organs, stress-activated signaling cascades alter chromatin, triggering maladaptive cell state transitions. Fibroblast activation is a common tissue stress response that worsens lung, liver, kidney and heart disease, yet its mechanistic basis remains obscure. Pharmacologic BET inhibition alleviates cardiac dysfunction, providing a tool to interrogate and modulate cardiac cell states as a potential therapeutic approach. Here, we leverage single-cell epigenomic interrogation of hearts dynamically exposed to BET inhibitors to reveal a reversible transcriptional switch underlying fibroblast activation. Resident cardiac fibroblasts demonstrated robust toggling between the quiescent and activated state in a manner directly correlating with BET inhibitor exposure and cardiac function. Single-cell chromatin accessibility revealed novel DNA elements whose accessibility dynamically correlated with cardiac performance. Among the most dynamic elements was an enhancer regulating the transcription factor MEOX1, which was specifically expressed in activated fibroblasts, occupied putative regulatory elements of a broad fibrotic gene program, and was required for TGFß-induced fibroblast activation. Selective CRISPR inhibition of the single most dynamic cis-element within the enhancer blocked TGFß-induced Meox1 activation. We identify MEOX1 as a central regulator of fibroblast activation associated with cardiac dysfunction, and also demonstrate its upregulation upon activation of human lung, liver and kidney fibroblasts. The plasticity and specificity of BET-dependent regulation of MEOX1 in tissue fibroblasts provide new trans- and cis- targets for treating fibrotic disease. Overall design: 2 replicates for each sample were run for both single cell RNA and ATAC seq (2x Sham, 2x TAC, 2x TAC JQ1, 2xTAC JQ1 withdrawn). 2 replicates for each sample were run for PRO seq (2x Unstimulated, 2x TGFb, 2x TGFb + siRNA Ctrl, 2x TGFb + siRNA Meox1). 1 replicate for each sample was ran for 4C (1x Unstimulated, 1x TGFb). 2 replicates for MEOX1 ChIPseq. 3 replicates for each sample for bulkRNAseq (3x Sham, 3x TAC, 3x TAC JQ1). 8 PROseq samples (2x Unstimulated, 2x TGFb, 2x TGFb + siRNA Ctrl, 2x TGFb + siRNA Meox1). 6 MEOX1 ChIPseq samples (3x for Unstim and 3x for TGFb-treated conditions). 4 H3K27ac ChIPseq samples (3x for Unstim and 3x for TGFb-treated conditions).
Sample: H3K27ac_Unstim_Rep2
SAMN17170376 • SRS7928879 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: NextSeq 500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: For ChIPseq experiment, cells were treated as follows: 10x106 FBs were pelleted (either in the Unstimulated or TGFb-treated conditions) and suspended in 10ml DMEM and cross-linked in 1% formalin solution (Thermo Fisher Scientific) by rocking in room temperature for 10 minutes. Then glycine (final concentration 0.125M) was added to quench the cross-link for 5minutes. Samples were centrifuged at 1000 rcf for 5minutes at 4C. Cells were washed with 10ml of cold 1x PBS supplemented with proteinase inhibitors and phosphatase inhibitors (Roche # 4693132001) and the pellets were snap frozen in liquid nitrogen. All samples were stored at -80C until use. When ready, cell pellets were incubated in cell lysis buffer (20 mM Tris-HCl, pH 8, 85 mM KCl, 0.5% NP-40, protease inhibitors for 10 min on a rotator at 4C. Nuclei were isolated by centrifugation (2,500 x g, 5 min, 4C), resuspended in nuclear lysis buffer (50 mM Tris-HCl, pH 8, 10 mM EDTA, pH 8, 1% SDS, protease inhibitors) and incubated on a rotator for 30 min at 4C. Chromatin was sheared using a Covaris S2 sonicator (Covaris Inc) for 20 min (60 s cycles, 20% duty cycle, 200 cycles/burst, intensity = 5) until DNA was in the 200–700 base-pair range. Chromatin was diluted 3-fold in ChIP dilution buffer (0.01% SDS, 1.1% Triton X-100, 1.2mMEDTA, 16.7mMTris-HCl, pH 8, 167 mM NaCl, protease inhibitors) and incubated with 2ul of anti-H3K27ac antibody (Abcam #ab4729) at 4C overnight under rotation. Antibody-protein complexes were immunoprecipitated using Pierce Protein A/G magnetic beads at 4C for 2 h under rotation. Beads were washed five times (2-min/wash under rotation) with cold RIPA buffer (50 mM HEPES- KOH, pH 7.5, 500 mM LiCl, 1 mM EDTA, 1% NP-40, 0.7% Na-deoxycholate), followed by one wash in cold final wash buffer (1xTE, 50 mM NaCl). Immunoprecipitated chromatin was eluted at 65C with agitation for 30 min in elution buffer (50mMTris-HCl pH 8.0, 10mMEDTA, 1% SDS). High-salt buffer (250mM Tris-HCl, pH 7.5, 32.5 mM EDTA, pH 8, 1.25M NaCl) and Proteinase K (New England Biolabs Inc (NEB)) were added and crosslinks were reversed overnight at 65C. Samples were treated with RNase A, and DNA was purified with AMPure XP beads (Beckman Coulter cat #A63881). Fragmented ChIP and input DNA were end-repaired, 5'-phosphorylated and dA-tailed with NEBNext Ultra II DNA Library Prep Kit for Illumina (NEB, E7645). Samples were ligated to adaptor oligos for multiplex sequencing (NEB, E7335), PCR amplified, and sequenced on an Illumina NextSeq 500 at the Gladstone Institutes.
Experiment attributes:
GEO Accession: GSM4990679
Links:
Runs: 1 run, 42.6M spots, 3.2G bases, 566.6Mb
Run# of Spots# of BasesSizePublished
SRR1331311242,621,3593.2G566.6Mb2021-04-09

ID:
12740420

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