Regulatory Factor X1 Downregulation Contributes to Monocyte Chemoattractant Protein-1 Overexpression in CD14+ Monocytes via Epigenetic Mechanisms in Coronary Heart Disease

Jia, Sujie; Yang, Shuang; Du, Pan; Gao, Keqin; Cao, Yu; Yao, Baige; Guo, Ren; Zhao, Ming

doi:10.3389/fgene.2019.01098

Cited by 11 publications

(6 citation statements)

References 43 publications

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“…4D ). Both of these cells types play crucial roles in vascular dysfunction 67 , while RFX factors are correlated with epigenetic changes in hypertension patients 68 and RFX1 indirectly reduces monocyte recruitment in atherosclerosis 69 . Given motif similarities between RFX factors, further work will be particularly important to understand the role of particular RFX TFs in endothelial and macrophage function.…”

Section: Resultsmentioning

confidence: 99%

Single-cell analysis of chromatin and expression reveals age- and sex-associated alterations in the human heart

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Daza

Booth

et al. 2022

Preprint

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Sex differences and age-related changes in the human heart at the tissue, cell, and molecular level have been well-documented and many may be relevant for cardiovascular disease. However, how molecular programs within individual cell types vary across individuals by age and sex remains poorly characterized. To better understand this variation, we performed single-nucleus combinatorial indexing (sci) ATAC- and RNA-Seq in human heart samples from nine donors. We identify hundreds of differentially expressed genes by age and sex. Sex dependent alterations include pathways such as TGFβ signaling and metabolic shifts by sex, evident in both transcriptional alterations and differing presence of transcription factor (TF) motifs in accessible chromatin. Age was associated with changes such as immune activation-related transcriptional and chromatin accessibility differences, as well as changes in the relative proportion of cardiomyocytes, neurons, and perivascular cells. In addition, we compare our adult-derived ATAC-Seq profiles to analogous fetal cell types to identify putative developmental-stage-specific regulatory factors. Finally, we train predictive models of cell-type-specific RNA expression levels utilizing ATAC-Seq profiles to link distal regulatory sequences to promoters, quantifying the predictive value of a simple TF-to-expression regulatory grammar and identifying cell-type-specific TFs.

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Section: Resultsmentioning

confidence: 99%

Single-cell analysis of chromatin and expression reveals age- and sex-associated alterations in the human heart

Read

Daza

Booth

et al. 2022

Preprint

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“…In coronary heart disease or coronary artery disease, RFX1 was shown to influence CD14 + monocytes via epigenetic processes, [48,49] whereas its role in bone metabolism-related diseases or the process of bone formation has not been fully investigated. Thus, we revealed a unique and crucial function for RFX-1 in the control of elevated IL-17A production in CD4 + T lymphocytes treated with MS, which encouraged osteogenic differentiation and angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Silicon‐Based Biomaterials Modulate the Adaptive Immune Response of T Lymphocytes to Promote Osteogenesis/Angiogenesis via Epigenetic Regulation

Xia,

Wu,

Chen

et al. 2023

Adv Healthcare Materials

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Silicon (Si)‐based biomaterials have been widely applied for bone regeneration. However, the underlying mechanisms of the materials function remain largely unknown. T lymphocyte‐mediated adaptive immune response plays a vital role in the process of bone regeneration. In the current study, mesoporous silica (MS) was used as a model material of Si‐based biomaterials. It showed that the supernatant of CD4+ T lymphocytes pretreated with MS extract significantly promoted the vascularized bone regeneration. The potential mechanism is closely related to the fact that MS extract could reduce the expression of regulatory factor X‐1 (RFX‐1) in CD4+ T lymphocytes. This might result in the overexpression of interleukin‐17A (IL‐17A) by boosting histone H3 acetylation and lowering DNA methylation and H3K9 trimethylation. Importantly, the in vivo experiments further revealed that MS particles significantly enhanced bone regeneration with improved angiogenesis in the critical‐sized calvarial defect mouse model accompanied by upregulation of IL‐17A in peripheral blood and the proportion of Th17 cells. Our study suggests that modulation of the adaptive immune response of T lymphocytes by Silicate‐based biomaterials plays an important role for bone regeneration.This article is protected by copyright. All rights reserved

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“…Studies have found that HDAC1 plays a vital role in cell proliferation and differentiation, cell cycle regulation as well as tissue transformation and development [ 22 – 26 ]. In addition, HDAC1 is found increased in various cancers, nervous system and heart diseases, and so on [ 27 – 29 ]. HDAC1 level is also elevated in lungs from human idiopathic PAH and rats with PAH; class I HDACs participate in the ECM remodeling of various tissues through different molecular mechanisms [ 8 , 9 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of HDAC1 alleviates monocrotaline-induced pulmonary arterial remodeling through up-regulation of miR-34a

Wang

et al. 2021

Respir Res

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Background It has been found that up-regulation of histone deacetylases 1 (HDAC1) is involved in the development of pulmonary arterial hypertension (PAH). However, it is still unclear whether inhibition of HDAC1 suppresses the development of PAH via restoring miR-34a level in monocrotaline (MCT)-induced PAH rats. Methods PAH rat models were induced by intraperitoneal injection of MCT. HDAC1 was suppressed by intraperitoneal injection of the class I HDAC inhibitor MS-275, and miR-34a was over-expressed via tail vein injection of miR-34a agomiR. Results HDAC1 protein was significantly increased in MCT-induced PAH rats; this was accompanied with down-regulation of miR-34a and subsequent up-regulation of matrix metalloproteinase 9 (MMP-9)/tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-2/TIMP-2. Administration of PAH rats with MS-275 or miR-34a agomiR dramatically abolished MCT-induced reduction of miR-34a and subsequent up-regulation of MMP-9/TIMP-1 and MMP-2/TIMP-2, finally reduced extracellular matrix (ECM) accumulation, pulmonary arterial remodeling, right ventricular systolic pressure (RVSP) and right ventricle hypertrophy index (RVHI) in PAH rats. Conclusions HDAC1 contributes to the development of MCT-induced rat PAH by suppressing miR-34a level and subsequently up-regulating the ratio of MMP-9/TIMP-1 and MMP-2/TIMP-2. Inhibition of HDAC1 alleviates pulmonary arterial remodeling and PAH through up-regulation of miR-34a level and subsequent reduction of MMP-9/TIMP-1 and MMP-2/TIMP-2, suggesting that inhibition of HDAC1 might have potential value in the management of PAH.

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Regulatory Factor X1 Downregulation Contributes to Monocyte Chemoattractant Protein-1 Overexpression in CD14+ Monocytes via Epigenetic Mechanisms in Coronary Heart Disease

Cited by 11 publications

References 43 publications

Single-cell analysis of chromatin and expression reveals age- and sex-associated alterations in the human heart

Single-cell analysis of chromatin and expression reveals age- and sex-associated alterations in the human heart

Silicon‐Based Biomaterials Modulate the Adaptive Immune Response of T Lymphocytes to Promote Osteogenesis/Angiogenesis via Epigenetic Regulation

Inhibition of HDAC1 alleviates monocrotaline-induced pulmonary arterial remodeling through up-regulation of miR-34a

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