PRMT7 targets of Foxm1 controls alveolar myofibroblast proliferation and differentiation during alveologenesis

He, Huacheng; Chen, Jilin; Zhao, Jian; Zhang, Peizhun; Qiao, Yulong; Wan, Hang; Wang, Jincheng; Mei, Mei; Bao, Shilai; Li, Qiuling

doi:10.1038/s41419-021-04129-1

Cited by 14 publications

(6 citation statements)

References 53 publications

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“…Researchers have also demonstrated that PRMT7-mediated histone arginine monomethylation activates Foxm1 transcriptional expression, which in turn regulates alveolar myofibroblast proliferation and differentiation. 28 PRMT7 facilitates the methylation of histone H4 arginine 3 (H4R3me1) to exert a repressive effect on Bcl6 expression. 31 Furthermore, PRMT7 promotes monomethylation of histones at the regulatory elements associated with RAP1A gene, leading to enhanced transcription responsible for monocyte adhesion and migration functions.…”

Section: ■ Discussionmentioning

confidence: 99%

“…PRMT7 is currently the sole documented type III enzyme accountable for arginine residue monomethylation on both histone and nonhistone substrates. Researchers have also demonstrated that PRMT7-mediated histone arginine monomethylation activates Foxm1 transcriptional expression, which in turn regulates alveolar myofibroblast proliferation and differentiation . PRMT7 facilitates the methylation of histone H4 arginine 3 (H4R3me1) to exert a repressive effect on Bcl6 expression .…”

Section: Discussionmentioning

confidence: 99%

“…Prmt7 knockout in mice resulted in a significant reduction of Hmgb2 expression in lung tissues, suggesting that Prmt7 may target and regulate Hmgb2. 28 Interestingly, Hmgb2 is known to be an important component of superenhancers and has been reported to promote the transcription of Acsl1, which is a novel inducer of ferroptosis. 29 Based on this information, we hypothesized that Prmt7 might regulate ferroptosis in SAP by activating the pathway involving Hmgb2 and Acsl1.…”

Section: Prmt7 Activates Hmgb2-acsl1 Pathway In Ar42j Cellsmentioning

confidence: 99%

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PRMT7-Dependent Transcriptional Activation of Hmgb2 Aggravates Severe Acute Pancreatitis by Promoting Acsl1-Induced Ferroptosis

Su,

Chen,

Han

et al. 2024

J. Proteome Res.

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Severe acute pancreatitis (SAP) is a highly fatal abdominal emergency, and its association with protein arginine methyltransferase 7 (PRMT7), the sole known type III enzyme responsible for the monomethylation of arginine residue, remains unexplored. In this study, we observe an increase in the PRMT7 levels in the pancreas of SAP mice and Cerulein-LPS-stimulated AR42J cells. Overexpression of Prmt7 exacerbated pancreatic damage in SAP, while the inhibition of PRMT7 improved SAP-induced pancreatic damage. Furthermore, PRMT7 overexpression promoted inflammation, oxidative stress, and ferroptosis during SAP. Mechanically, PRMT7 catalyzed monomethylation at histone H4 arginine 3 (H4R3me1) at the promoter region of high mobility group proteins 2 (HMGB2), thereby enhancing its transcriptional activity. Subsequently, HMGB2 facilitated Acyl CoA synthase long-chain family member 1 (ACSL1) transcription by binding to its promoter region, resulting in the activation of ferroptosis. Inhibition of PRMT7 effectively alleviated ferroptosis in Cerulein-LPS-induced AR42J cells by suppressing the HMGB2-ACSL1 pathway. Overall, our study reveals that PRMT7 plays a crucial role in promoting SAP through its regulation of the HMGB2-ACSL1 pathway to accelerate ferroptosis.

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Section: ■ Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Prmt7 Activates Hmgb2-acsl1 Pathway In Ar42j Cellsmentioning

confidence: 99%

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PRMT7-Dependent Transcriptional Activation of Hmgb2 Aggravates Severe Acute Pancreatitis by Promoting Acsl1-Induced Ferroptosis

Su,

Chen,

Han

et al. 2024

J. Proteome Res.

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“…Mouse AMYFs were isolated from wild-type C57BL/6J mice as previously described [21]. Raw264.7 cells were purchased from IMMOCELL (Xiamen, China).…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Deficiency of SPP1 alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice

Liu,

Bao,

Zhou

et al. 2024

Preprint

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Bronchopulmonary dysplasia (BPD) is a common chronic lung disorder characterized by impaired proximal airway and bronchoalveolar development in premature births. SPP1 is involved in lung development and lung injury events, while its role was not explored in BPD. In the current study, the hyperoxiainduced lung injury animal models were generated by exposing neonatal mice to hyperoxia for 7 days after birth, and alveolar myofibroblasts (AMYFs) were treated with hyperoxia to establish the in vitro models of BPD. Based on the scRNA-seq analysis of lungs of mice housed under normoxia or hyperoxia conditions, mouse macrophages and fibroblasts were main different cell clusters between the two groups, and differentially expressed genes in fibroblasts were screened. Further GO and KEGG enrichment analysis revealed that these differentially expressed genes were mainly enriched in the pathways related to cell proliferation, apoptosis as well as the PI3K-AKT and ERK/MAPK pathways. SPP1 was found up-regulated in the lung tissues of hyperoxia mice. We also demonstrated the up-regulation of SPP1 in the BPD patients as well as hyperoxiainduced lung injury mouse models and cells. SPP1 deficiency was revealed to reduce the hyperoxia-induced apoptosis, oxidative stress and inflammation and increase the viability of AMYFs. In the hyperoxiainduced lung injury mouse models, SPP1 deficiency was demonstrated to reverse the hyperoxia-induced alveolar growth disruption, oxidative stress and inflammation. Overall, SPP1 exacerbates BPD progression in vitro and in vivo by regulating oxidative stress and inflammatory response via the PI3K-AKT and ERK/MAPK pathways, which might provide novel therapeutic target for BPD therapy.

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“…According to their modulation mode, CRs can be divided into three categories: DNA methylators, histone modifiers, and chromatin remodelers (7). Current studies have reported that CRs can affect the progress of IPF by modulating the proliferation and differentiation of alveolar myofibroblasts and regulating apoptosis (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Bioinformatic identification and analysis of immune-related chromatin regulatory genes as potential biomarkers in idiopathic pulmonary fibrosis

Li¹,

Liu²,

Zhang³

et al. 2022

Ann Transl Med

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Background: Idiopathic pulmonary fibrosis (IPF) is a disease with a very poor prognosis. The search for new IPF biomarkers is particularly urgent due to the uncertainty of the mechanisms and treatment. Studies have shown that CRs are involved in the development of IPF and are associated with tumor immunity.However, there are no studies on immune-related CRs in IPF. Therefore, we conducted a systematic study to analyze the expression levels and immune correlation of CRs in IPF tissues and normal tissues and to explore their potential as diagnostic biomarkers.Methods: GSE53845, GSE179781 and GSE24206 datasets from Gene Expression Omnibus (GEO) database were merged into an integrated dataset as the training set; GSE70866 was used as the validation dataset. The cr-related differentially expressed genes (DEGs) between normal and IPF tissues were identified using the "Limma" software package. Weighted gene co-expression network analysis (WGCNA) was performed using the "WGCNA" package to screen eigengenes, which were intersected with DEGs to identify hub genes. The "ggcorrplot" package was used to analyze the correlation between hub genes and immunity, and immune-related hub genes were defined as immHub. A logistic regression model was constructed using immHub as the independent variable and whether the diagnosis was IPF as the dependent variable.Results: One hundred and sixty-nine DEGs were identified between IPF and normal tissues. wGCNA identified 3 key modules in brown, green and yellow genes that were present in all 3 modules and met module membership (MM) >0.8 and gene significance (GS) >0.5 were called signature genes (n=390). four intersecting genes were obtained by intersecting DEGs with signature genes (PADI4, IGFBP7, GADD45A, and SETBP1) all associated with immunity were defined as immHub genes Logistic regression models were constructed based on immHub genes. The area under the curve (AUC) of the ROC curve is used to evaluate the diagnostic accuracy of the logistic regression model for IPF. The AUC in the ROC analysis was 0.771 for the training dataset, and 0.759 for the validation dataset.Conclusions: PADI4, IGFBP7 and GADD45A may be biomarkers for IPF, which will provide assistance in the diagnosis, treatment and prognostic assessment of IPF patients, and provide an important basis for future studies on the relationship between CRS genes and IPF.

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PRMT7 targets of Foxm1 controls alveolar myofibroblast proliferation and differentiation during alveologenesis

Cited by 14 publications

References 53 publications

PRMT7-Dependent Transcriptional Activation of Hmgb2 Aggravates Severe Acute Pancreatitis by Promoting Acsl1-Induced Ferroptosis

PRMT7-Dependent Transcriptional Activation of Hmgb2 Aggravates Severe Acute Pancreatitis by Promoting Acsl1-Induced Ferroptosis

Deficiency of SPP1 alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice

Bioinformatic identification and analysis of immune-related chromatin regulatory genes as potential biomarkers in idiopathic pulmonary fibrosis

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