BACH1 Deficiency Prevents Neointima Formation and Maintains the Differentiated Phenotype of Vascular Smooth Muscle Cell by Regulating Chromatin Accessibility
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ABSTRACT:
PROVIDER: PRJNA764432 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21815040_1.fastq.gz | Fastqsanger.gz | |||
| SRR21815040_2.fastq.gz | Fastqsanger.gz | |||
| SRR21815041_1.fastq.gz | Fastqsanger.gz | |||
| SRR21815041_2.fastq.gz | Fastqsanger.gz | |||
| SRR21815042_1.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin accessibility is important for cell fate determination in differentiation and multiple pathophysiological processes. Here, we report a transcription factor BACH1, facilitates the recruitment of G9a and YAP, maintains the state of H3K9me2 and decreases the chromatin accessibility at the promoter of VSMC marker genes, thereby repressing their expression and contributing to dedifferentiated VSMC phenotype. Moreover, VSMC-specific loss of BACH1 in mice inhibited the transformation of VSMC from contractile to synthetic phenotype and VSMC proliferation and attenuated the neointimal hyperplasia in wire-injured femoral arteries.
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Project description:Vascular smooth muscle cells (VSMCs) derived from human embryonic stem cells (hESCs) have been considered as a potential therapeutic application in vascular diseases. The transcription factor BTB and CNC homology 1 (BACH1) participates in stem cell development and has an increased expression during the VSMCs differentiation process. Knockout of BACH1 inhibits the differentiation of hESCs into VSMCs, whereas overexpression of BACH1 promotes VSMCs differentiation after the mesoderm stage. Mechanistically, BACH1 interacts with Coactivator-associated arginine methyltransferase 1 (CARM1) in a bZIP domain-dependent manner. BACH1 recruits CARM1 and its specific histone mark H3R17me2 to VSMC marker genes promoters, thus up-regulating target gene expression. BACH1-induced promotion of VSMC marker genes was partially abolished by the knockdown of CARM1 or H3R17me2. Thus, our results demonstrate the regulatory role of BACH1 and CARM1 in VSMCs differentiation.
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Project description:Maintenance of stem-cell identity requires proper regulation of enhancer activity. Both transcription factors OCT4/SOX2/NANOG and histone methyltransferase complexes MLL/SET1 were shown to regulate enhancer activity, but how they are regulated in embryonic stem cells (ESCs) remains further studies. Here, we report a transcription factor BACH1, who which directly interacts with OCT4/SOX2/NANOG (OSN) and MLL/SET1 methyltransferase complexes and maintains pluripotency in mouse ESCs (mESCs). BTB domain and bZIP domain of BACH1 are required for these interactions and pluripotency maintenance. Loss of BACH1 reduced the interaction between NANOG and MLL1/SET1 complexes, and decreased their occupancy on chromatin, and further decreased H3 lysine 4 trimethylation (H3K4me3) level on gene promoters and (super-) enhancers, leading to decreased enhancer activity and transcription activity, especially on stemness-related genes. Moreover, BACH1 recruited NANOG through chromatin looping and regulated remote NANOG binding, fine-tuning enhancer-promoter activity and gene expression. Collectively, these observations suggest that BACH1 maintains pluripotency in ESCs by recruiting NANOG and MLL/SET1 complexes to chromatin and maintaining the trimethylated state of H3K4 and enhancer-promoter activity, especially on stemness-related genes.
2021-01-12 | GSE142519 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.
2011-05-13 | E-GEOD-28051 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE28050: Expression data from knockdown of BACH1 in HEK 293T cells GSE28051: Genome-wide map of BACH1 binding in HEK293T cells Refer to individual Series
2011-05-12 | E-GEOD-28053 | biostudies-arrayexpress
Project description:Genes regulated by Bach1 transcription factor
2012-07-09 | E-MEXP-3674 | biostudies-arrayexpress
Project description:Vascular smooth muscle cell (VSMC) migration and proliferation are critical events in the development of neointima following vascular injury. Exogenous expression of human CD9 by CD9-adenoviral transduction led to increases in neointima. CD9 expression significantly augmented PI-3 kinase dependent Akt phosphorylation with concurrent adhesion to extracellular matrix protein fibronectin (FN). Furthermore,enhanced Akt phosphorylation was attenuated by anti-CD9 mAb7 binding. As multiple factors contribute to the regulation of VSMC phenotype, our aim was to establish whether increased CD9 expression would induce changes in the expression of other genes associated with VSMC proliferation and motility. RASM were transduced with either CD9 adenovirus or control and were plated on FN for 6hours. Cells were harvested from 3 replicate plates and total RNA from each was isolated using the TRIzol method and pooled for each CD9 and LacZ transduced RASM. RNA was sent to Genome Explorations Memphis TN for microarray analysis. Microarray analyses were done using the U230.2 rat gene chip from Affymetrix using RNA prepared from two RASM transduction experiments. Two independent microarray data sets have been generated and analyzed by comparing the filtered gene lists generated by the Affymetrix GeneChip Operating Software and looking for regulated genes common both sets of data. Analysis of this data showed the regulation of some key genes involved in the modulation of VSMC motility and proliferation. Keywords: vascular smooth muscle cells, vascular injury, tetraspanin, proliferation, neointima, motility, fibronectin (FN), rat aortic smooth muscle (RASM)
2009-11-12 | GSE13594 | GEO
Project description:We identify transcription factor BACH1 as a master regulator in vascular cells during aging. BACH1 is upregulated in the aorta of old mice. We find BACH1 is located on open chromatin and BACH1 binds to CDKN1A gene enhancer and activates its transcription in endothelial cells. Finally, BACH1 aggravates endothelial cell senescence under oxidative stress. Thus, these findings demonstrate a crucial regulatory role of BACH1 in vascular aging.
2024-09-15 | GSE185210 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis.
2011-05-13 | GSE28051 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we performed knock-down of BACH1 in HEK 293T cells using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. Knockdown of BACH1 in HEK 293T cells was carried out with three different types of siRNA molecules (esiRNA = e, siRNA1 SI00309876 from Qiagen = q and Stealth siRNA2 HSS100910 from Invitrogen = s), followed by RNA extraction after 24h and 72h of knockdown and hybridization on Affymetrix microarrays. For each siRNA type, we performed the experiments in triplicates, with four control replicates (mock transfections without siRNA) at 24h and three control replicates at 72h, resulting in nine samples and four controls at 24h and nine samples and three controls at 72h. Samples at 24h of knockdown: e_1_24, e_2_24, e_3_24, q_1_24, q_2_24, q_3_24, s_1_24, s_2_24, s_3_24. Controls at 24h: m_1_24, m_2_24, m_3_24, m_4_72. Samples at 72h of knockdown: e_1_72, e_2_72, e_3_72, q_1_72, q_2_72, q_3_72, s_1_72, s_2_72, s_3_72. Controls at 72h: m_1_72, m_2_72, m_3_72. REPEATS: biological replicate: BACH1_e_1_24, BACH1_e_2_24, BACH1_e_3_24 biological replicate: BACH1_q_1_24, BACH1_q_2_24, BACH1_q_3_24 biological replicate: BACH1_s_1_24, BACH1_s_2_24, BACH1_s_3_24 biological replicate: BACH1_m_1_24, BACH1_m_2_24, BACH1_m_3_24, BACH1_m_4_24 biological replicate: BACH1_e_1_72, BACH1_e_2_72, BACH1_e_3_72 biological replicate: BACH1_q_1_72, BACH1_q_2_72, BACH1_q_3_72 biological replicate: BACH1_s_1_72, BACH1_s_2_72, BACH1_s_3_72 biological replicate: BACH1_m_1_72, BACH1_m_2_72, BACH1_m_3_72
2011-05-13 | E-GEOD-28050 | biostudies-arrayexpress