Myeloid Zinc Finger 1 (MZF‐1) Regulates Expression of the <i>CCN2/CTGF</i> and <i>CCN3/NOV</i> Genes in the Hematopoietic Compartment

Piszczatowski, Richard T.; Rafferty, B.; Rozado, Andre; Parziale, James V.; Lents, Nathan H.

doi:10.1002/jcp.25021

Cited by 9 publications

(5 citation statements)

References 36 publications

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“…In the present study, the CpG 2–4 and CpG17–18 were all located within 100 bp of the TSS. The CpG 2–4 and CpG 17–18 co-localise with 3 putative transcription factors, which are involved in cell proliferation and differentiation (TFAP2A) [ 23 ], cell cycle (E2F4) [ 24 ] and hematopoiesis (MZF1) [ 25 ]. We also found that an experimentally validated transcription factor ELK1 was bound to CpG 6, which was located 19 bp upstream of TSS and 24 bp downstream of CpG 2–4, and had higher methylation in benzene-exposed workers than unexposed controls, although the difference was not significant.…”

Section: Discussionmentioning

confidence: 99%

Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity

Zheng

Lin²,

Hou³

et al. 2017

IJERPH

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Benzene is a primary industrial chemical and a ubiquitous environmental pollutant. ERCC3 is a key player in nucleotide excision repair. Recent studies suggested that site-specific methylation is a possible mechanism of the transcriptional dysregulation by blocking transcription factors binding. We previously found that the average promoter methylation level of ERCC3 was increased in benzene-exposed workers. In order to test whether specific CpG sites of ERCC3 play an important role in benzene-induced epigenetic changes and whether the specific methylation patterns are associated with benzene hematotoxicity, we analyzed the promoter methylation levels of individual CpG sites, transcription factor binding motif and the correlation between aberrant CpG methylation and hematotoxicity in 76 benzene-exposed workers and 24 unexposed controls in China. Out of all the CpGs analyzed, two CpG units located 43 bp upstream and 99 bp downstream of the transcription start site of ERCC3 (CpG 2–4 and CpG 17–18, respectively), showed the most pronounced increase in methylation levels in benzene-exposed workers, compared with unexposed controls (Mean ± SD: 5.86 ± 2.77% vs. 4.92 ± 1.53%, p = 0.032; 8.45 ± 4.09% vs. 6.79 ± 2.50%, p = 0.024, respectively). Using the JASPAR CORE Database, we found that CpG 2–4 and CpG 17–18 were bound by three putative transcription factors (TFAP2A, E2F4 and MZF1). Furthermore, the methylation levels for CpG 2–4 were correlated negatively with the percentage of neutrophils (β = −0.676, p = 0.005) in benzene-exposed workers. This study demonstrates that CpG-specific DNA methylation in the ERCC3 promoter region may be involved in benzene-induced epigenetic modification and it may contribute to benzene-induced hematotoxicity.

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Section: Discussionmentioning

confidence: 99%

Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity

Zheng

Lin²,

Hou³

et al. 2017

IJERPH

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“…18 Myeloid zinc finger 1 (MZF1) is a transcription factor of many genes ie c-Myc, connective tissue growth factor (CTGF), and MZF1 can obviously promote cell proliferation and ECM synthesis. [19][20][21] In the initial stage of this study, we not only revealed a potential MZF1-binding site in the promoter of RGC-32 gene, but also proved that the MZF1 expression increased simultaneously with RGC-32 both in vivo and in vitro. Therefore, the role of MZF1 and the relationship between MZF1 and RGC-32 in GMC proliferation and ECM production upon sublytic C5b-9 stimulation need to be clarified.…”

Section: Introductionmentioning

confidence: 52%

“…As we know, gene expression is often regulated by special transcriptional factors . Myeloid zinc finger 1 (MZF1) is a transcription factor of many genes ie c‐Myc, connective tissue growth factor (CTGF), and MZF1 can obviously promote cell proliferation and ECM synthesis . In the initial stage of this study, we not only revealed a potential MZF1‐binding site in the promoter of RGC‐32 gene, but also proved that the MZF1 expression increased simultaneously with RGC‐32 both in vivo and in vitro.…”

Section: Introductionmentioning

confidence: 99%

Sublytic C5b‐9 induces proliferation of glomerular mesangial cells via ERK5/MZF1/RGC‐32 axis activated by FBXO28‐TRAF6 complex

Wang

Zhao

et al. 2019

J Cellular Molecular Medi

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Mesangioproliferative glomerulonephritis (MsPGN) is characterized by the proliferation of glomerular mesangial cells (GMCs) and accumulation of extracellular matrix (ECM), followed by glomerulosclerosis and renal failure of patients. Although our previous studies have demonstrated that sublytic C5b‐9 complex formed on the GMC membrane could trigger GMC proliferation and ECM expansion of rat Thy‐1 nephritis (Thy‐1N) as an animal model of MsPGN, their mechanisms are still not fully elucidated. In the present studies, we found that the levels of response gene to complement 32 (RGC‐32), myeloid zinc finger 1 (MZF1), phosphorylated extracellular signal‐regulated kinase 5 (phosphorylated ERK5, p‐ERK5), F‐box only protein 28 (FBXO28) and TNF receptor‐associated factor 6 (TRAF6) were all markedly up‐regulated both in the renal tissues of rats with Thy‐1N (in vivo) and in the GMCs upon sublytic C5b‐9 stimulation (in vitro). Further in vitro experiments revealed that up‐regulated FBXO28 and TRAF6 could form protein complex binding to ERK5 and enhance ERK5 K63‐ubiquitination and subsequent phosphorylation. Subsequently, ERK5 activation contributed to MZF1 expression and MZF1‐dependent RGC‐32 up‐regulation, finally resulting in GMC proliferative response. Furthermore, the MZF1‐binding element within RGC‐32 promoter and the functions of FBXO28 domains were identified. Additionally, knockdown of renal FBXO28, TRAF6, ERK5, MZF1 and RGC‐32 genes respectively markedly reduced GMC proliferation and ECM production in Thy‐1N rats. Together, these findings indicate that sublytic C5b‐9 induces GMC proliferative changes in rat Thy‐1N through ERK5/MZF1/RGC‐32 axis activated by the FBXO28‐TRAF6 complex, which might provide a new insight into MsPGN pathogenesis.

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“…Myeloid Zinc Finger 1 (MZF‐1) is a hematopoietic transcription factor found in several cell types to interact with the CCN3 promoter and regulate the expression of CCN3. Notably, vitamin D3 and trans‐retinoic acid can induce the upregulation of CCN3 by MZF‐1 (Piszczatowski et al 2015). Several studies have identified the post‐transcriptional regulation of CCN3 by several micro RNAs (miRNAs).…”

Section: The Expression Regulation Mechanism Of Ccn3mentioning

confidence: 99%

The advance of CCN3 in fibrosis

Yin

Liu

Zhou

et al. 2023

J. Cell Commun. Signal.

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The extracellular matrix (ECM) is comprised of various extracellular macromolecules, including collagen, enzymes, and glycoproteins, which offer structural and biochemical support to neighboring cells. After tissue injury, extracellular matrix proteins deposit in the damaged tissue to promote tissue healing. However, an imbalance between ECM production and degradation can result in excessive deposition, leading to fibrosis and subsequent organ dysfunction. Acting as a regulatory protein within the extracellular matrix, CCN3 plays a crucial role in numerous biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Many studies have demonstrated that CCN3 can reduce the production of ECM in tissues through diverse mechanisms thereby exerting an inhibitory effect on fibrosis. Consequently, CCN3 emerges as a promising therapeutic target for ameliorating fibrosis.

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Myeloid Zinc Finger 1 (MZF‐1) Regulates Expression of the CCN2/CTGF and CCN3/NOV Genes in the Hematopoietic Compartment

Cited by 9 publications

References 36 publications

Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity

Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity

Sublytic C5b‐9 induces proliferation of glomerular mesangial cells via ERK5/MZF1/RGC‐32 axis activated by FBXO28‐TRAF6 complex

The advance of CCN3 in fibrosis

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