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Article ; Online: DNA methyltransferase inhibition induces dynamic gene expression changes in lung CD4

Michki, Nigel S / Ndeh, Roland / Helmin, Kathryn A / Singer, Benjamin D / McGrath-Morrow, Sharon A

2023 Volume 13, Issue 1, Page(s) 4283

Abstract: Bacterial pulmonary infections are a major cause of morbidity and mortality in neonates, with less severity in older children. Previous studies demonstrated that the DNA of ... ...

Abstract	Bacterial pulmonary infections are a major cause of morbidity and mortality in neonates, with less severity in older children. Previous studies demonstrated that the DNA of CD4
MeSH term(s)	Animals ; Mice ; T-Lymphocytes/metabolism ; Escherichia coli/genetics ; Animals, Newborn ; Lung/metabolism ; Pneumonia, Bacterial/metabolism ; DNA Modification Methylases/genetics ; Escherichia coli Infections/genetics ; DNA Methylation ; CD4-Positive T-Lymphocytes ; Gene Expression
Chemical Substances	DNA Modification Methylases (EC 2.1.1.-)
Language	English
Publishing date	2023-03-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-31285-5
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Article ; Online: CoRESTed development of regulatory T cells.

Morales-Nebreda, Luisa / Helmin, Kathryn A / Singer, Benjamin D

The Journal of clinical investigation

2020 Volume 130, Issue 4, Page(s) 1618–1621

Abstract: Tregs require specific epigenetic signatures to induce and maintain their suppressive function in the context of inflammation and cancer surveillance. In this issue of the JCI, Xiong and colleagues identify a critical role for the epigenetic repressor ... ...

Abstract	Tregs require specific epigenetic signatures to induce and maintain their suppressive function in the context of inflammation and cancer surveillance. In this issue of the JCI, Xiong and colleagues identify a critical role for the epigenetic repressor REST corepressor 1 (CoREST) in promoting Treg suppressive transcriptional and functional programs. Pharmacologic inhibition and genetic loss of CoREST in Tregs impaired organ allograft tolerance and unleashed antitumor immunity via epigenetic activation of effector T cell programs. We propose that exploiting epigenetic control mechanisms will further the translation of Treg-based therapeutics to target inflammatory and malignant disorders.
MeSH term(s)	Co-Repressor Proteins ; Epigenesis, Genetic ; T-Lymphocytes, Regulatory ; Transcription Factors ; Transplantation Tolerance
Chemical Substances	Co-Repressor Proteins ; Transcription Factors
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI135713
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Article ; Online: Transcriptional profiling of peripheral blood mononuclear cells identifies inflammatory phenotypes in Ataxia Telangiectasia.

Michki, Nigel S / Singer, Benjamin D / Perez, Javier V / Thomas, Aaron J / Natale, Valerie / Helmin, Kathryn A / Wright, Jennifer / Cheng, Leon / Young, Lisa R / Lederman, Howard M / McGrath-Morrow, Sharon A

Orphanet journal of rare diseases

2024 Volume 19, Issue 1, Page(s) 67

Abstract: Introduction: Ataxia telangiectasia (A-T) is an autosomal recessive neurodegenerative disease with widespread systemic manifestations and marked variability in clinical phenotypes. In this study, we sought to determine whether transcriptomic profiling ... ...

Abstract	Introduction: Ataxia telangiectasia (A-T) is an autosomal recessive neurodegenerative disease with widespread systemic manifestations and marked variability in clinical phenotypes. In this study, we sought to determine whether transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) defines subsets of individuals with A-T beyond mild and classic phenotypes, enabling identification of novel features for disease classification and treatment response to therapy. Methods: Participants with classic A-T (n = 77), mild A-T (n = 13), and unaffected controls (n = 15) were recruited from two outpatient clinics. PBMCs were isolated and bulk RNAseq was performed. Plasma was also isolated in a subset of individuals. Affected individuals were designated mild or classic based on ATM mutations and clinical and laboratory features. Results: People with classic A-T were more likely to be younger and IgA deficient and to have higher alpha-fetoprotein levels and lower % forced vital capacity compared to individuals with mild A-T. In classic A-T, the expression of genes required for V(D)J recombination was lower, and the expression of genes required for inflammatory activity was higher. We assigned inflammatory scores to study participants and found that inflammatory scores were highly variable among people with classic A-T and that higher scores were associated with lower ATM mRNA levels. Using a cell type deconvolution approach, we inferred that CD4 + T cells and CD8 + T cells were lower in number in people with classic A-T. Finally, we showed that individuals with classic A-T exhibit higher SERPINE1 (PAI-1) mRNA and plasma protein levels, irrespective of age, and higher FLT4 (VEGFR3) and IL6ST (GP130) plasma protein levels compared with mild A-T and controls. Conclusion: Using a transcriptomic approach, we identified novel features and developed an inflammatory score to identify subsets of individuals with different inflammatory phenotypes in A-T. Findings from this study could be used to help direct treatment and to track treatment response to therapy.
MeSH term(s)	Humans ; Ataxia Telangiectasia/genetics ; Ataxia Telangiectasia/metabolism ; Leukocytes, Mononuclear/metabolism ; Neurodegenerative Diseases/metabolism ; Phenotype ; Blood Proteins/genetics ; Blood Proteins/metabolism ; RNA, Messenger/metabolism
Chemical Substances	Blood Proteins ; RNA, Messenger
Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-024-03073-5
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Article: AMP-activated protein kinase is necessary for Treg cell functional adaptation to microenvironmental stress.

Torres Acosta, Manuel A / Mambetsariev, Nurbek / Reyes Flores, Carla P / Helmin, Kathryn A / Liu, Qianli / Joudi, Anthony M / Morales-Nebreda, Luisa / Gurkan, Jonathan / Cheng, Kathleen / Abdala-Valencia, Hiam / Weinberg, Samuel E / Singer, Benjamin D

bioRxiv : the preprint server for biology

2023

Abstract: CD4+FOXP3+ regulatory T (Treg) cells maintain self-tolerance, suppress the immune response to cancer, and protect against tissue injury in the lung and other organs. Treg cells require mitochondrial metabolism to exert their function, but how Treg cells ... ...

Abstract	CD4+FOXP3+ regulatory T (Treg) cells maintain self-tolerance, suppress the immune response to cancer, and protect against tissue injury in the lung and other organs. Treg cells require mitochondrial metabolism to exert their function, but how Treg cells adapt their metabolic programs to sustain and optimize their function during an immune response occurring in a metabolically stressed microenvironment remains unclear. Here, we tested whether Treg cells require the energy homeostasis-maintaining enzyme AMP-activated protein kinase (AMPK) to adapt to metabolically aberrant microenvironments caused by malignancy or lung injury, finding that AMPK is dispensable for Treg cell immune-homeostatic function but is necessary for full Treg cell function in B16 melanoma tumors and during acute lung injury caused by influenza virus pneumonia. AMPK-deficient Treg cells had lower mitochondrial mass and exhibited an impaired ability to maximize aerobic respiration. Mechanistically, we found that AMPK regulates DNA methyltransferase 1 to promote transcriptional programs associated with mitochondrial function in the tumor microenvironment. In the lung during viral pneumonia, we found that AMPK sustains metabolic homeostasis and mitochondrial activity. Induction of DNA hypomethylation was sufficient to rescue mitochondrial mass in AMPK-deficient Treg cells, linking DNA methylation with AMPK function and mitochondrial metabolism. These results define AMPK as a determinant of Treg cell adaptation to metabolic stress and offer potential therapeutic targets in cancer and tissue injury.
Language	English
Publishing date	2023-12-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.29.568904
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Article: mTORC1 stimulates cell growth through SAM synthesis and m6A mRNA-dependent control of protein synthesis

Villa, Elodie / Sahu, Umakant / O’Hara, Brendan P / Ali, Eunus S / Helmin, Kathryn A / Asara, John M / Gao, Peng / Singer, Benjamin D / Ben-Sahra, Issam

Molecular cell. 2021 May 20, v. 81, no. 10

2021

Abstract: The mechanistic target of rapamycin complex 1 (mTORC1) regulates metabolism and cell growth in response to nutrient, growth, and oncogenic signals. We found that mTORC1 stimulates the synthesis of the major methyl donor, S-adenosylmethionine (SAM), ... ...

Abstract	The mechanistic target of rapamycin complex 1 (mTORC1) regulates metabolism and cell growth in response to nutrient, growth, and oncogenic signals. We found that mTORC1 stimulates the synthesis of the major methyl donor, S-adenosylmethionine (SAM), through the control of methionine adenosyltransferase 2 alpha (MAT2A) expression. The transcription factor c-MYC, downstream of mTORC1, directly binds to intron 1 of MAT2A and promotes its expression. Furthermore, mTORC1 increases the protein abundance of Wilms’ tumor 1-associating protein (WTAP), the positive regulatory subunit of the human N⁶-methyladenosine (m⁶A) RNA methyltransferase complex. Through the control of MAT2A and WTAP levels, mTORC1 signaling stimulates m⁶A RNA modification to promote protein synthesis and cell growth. A decline in intracellular SAM levels upon MAT2A inhibition decreases m⁶A RNA modification, protein synthesis rate, and tumor growth. Thus, mTORC1 adjusts m⁶A RNA modification through the control of SAM and WTAP levels to prime the translation machinery for anabolic cell growth.
Keywords	RNA ; S-adenosylmethionine ; cell growth ; humans ; introns ; methionine adenosyltransferase ; methyltransferases ; neoplasms ; protein synthesis ; rapamycin ; transcription factors
Language	English
Dates of publication	2021-0520
Size	p. 2076-2093.e9.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.03.009
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: ELOA3

Morgan, Marc A J / Mohammad Parast, Saeid / Iwanaszko, Marta / Aoi, Yuki / Yoo, DongAhn / Dumar, Zachary J / Howard, Benjamin C / Helmin, Kathryn A / Liu, Qianli / Thakur, William R / Zeidner, Jacob M / Singer, Benjamin D / Eichler, Evan E / Shilatifard, Ali

Science advances

2023 Volume 9, Issue 47, Page(s) eadj1261

Abstract: The biological role of the repetitive DNA sequences in the human genome remains an outstanding question. Recent long-read human genome assemblies have allowed us to identify a function for one of these repetitive regions. We have uncovered a tandem array ...

Abstract	The biological role of the repetitive DNA sequences in the human genome remains an outstanding question. Recent long-read human genome assemblies have allowed us to identify a function for one of these repetitive regions. We have uncovered a tandem array of conserved primate-specific retrogenes encoding the protein Elongin A3 (ELOA3), a homolog of the RNA polymerase II (RNAPII) elongation factor Elongin A (ELOA). Our genomic analysis shows that the
MeSH term(s)	Animals ; Humans ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; Peptide Elongation Factors/genetics ; Primates/genetics ; Elongin/genetics ; Multigene Family ; Tandem Repeat Sequences/genetics
Chemical Substances	RNA Polymerase II (EC 2.7.7.-) ; Peptide Elongation Factors ; Elongin
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adj1261
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Article ; Online: Multidimensional assessment of alveolar T cells in critically ill patients.

Walter, James M / Helmin, Kathryn A / Abdala-Valencia, Hiam / Wunderink, Richard G / Singer, Benjamin D

JCI insight

2018 Volume 3, Issue 17

Abstract: Pneumonia represents the leading infectious cause of death in the United States. Foxp3+ regulatory T cells promote recovery from severe pneumonia in mice, but T cell responses in patients with pneumonia remain incompletely characterized because of the ... ...

Abstract	Pneumonia represents the leading infectious cause of death in the United States. Foxp3+ regulatory T cells promote recovery from severe pneumonia in mice, but T cell responses in patients with pneumonia remain incompletely characterized because of the limited ability to serially sample the distal airspaces and perform multidimensional molecular assessments on the small numbers of recovered cells. As T cell function is governed by their transcriptional and epigenetic landscape, we developed a method to safely perform high-resolution transcriptional and DNA methylation profiling of T cell subsets from the alveoli of critically ill patients. Our method involves nonbronchoscopic bronchoalveolar lavage combined with multiparameter fluorescence-activated cell sorting, unsupervised low-input RNA-sequencing, and a modified reduced-representation bisulfite sequencing protocol. Here, we demonstrate the safety and feasibility of our method and use it to validate functional genomic elements that were predicted by mouse models. Because of its potential for widespread application, our techniques allow unprecedented insights into the biology of human pneumonia.
MeSH term(s)	Animals ; Critical Illness ; DNA Methylation ; Epigenomics ; Forkhead Transcription Factors ; Humans ; Mice ; Pneumonia/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Regulatory ; Transcriptome
Chemical Substances	Forkhead Transcription Factors ; Foxp3 protein, mouse
Language	English
Publishing date	2018-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.123287
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Article ; Online: SIRT3 Overexpression Ameliorates Asbestos-Induced Pulmonary Fibrosis, mt-DNA Damage, and Lung Fibrogenic Monocyte Recruitment.

Cheresh, Paul / Kim, Seok-Jo / Jablonski, Renea / Watanabe, Satoshi / Lu, Ziyan / Chi, Monica / Helmin, Kathryn A / Gius, David / Budinger, G R Scott / Kamp, David W

International journal of molecular sciences

2021 Volume 22, Issue 13

Abstract: Alveolar epithelial cell (AEC) mitochondrial (mt) DNA damage and fibrotic monocyte-derived alveolar macrophages (Mo-AMs) are implicated in the pathobiology of pulmonary fibrosis. We showed that sirtuin 3 (SIRT3), a mitochondrial protein regulating cell ... ...

Abstract	Alveolar epithelial cell (AEC) mitochondrial (mt) DNA damage and fibrotic monocyte-derived alveolar macrophages (Mo-AMs) are implicated in the pathobiology of pulmonary fibrosis. We showed that sirtuin 3 (SIRT3), a mitochondrial protein regulating cell fate and aging, is deficient in the AECs of idiopathic pulmonary fibrosis (IPF) patients and that asbestos- and bleomycin-induced lung fibrosis is augmented in Sirt3 knockout (
MeSH term(s)	Animals ; Asbestos/adverse effects ; Biomarkers ; DNA Damage ; DNA, Mitochondrial ; Disease Models, Animal ; Gene Expression ; Humans ; Idiopathic Pulmonary Fibrosis/etiology ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Immunohistochemistry ; Mice ; Mice, Transgenic ; Mitochondria/genetics ; Mitochondria/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Monocytes/pathology ; Oxidative Stress ; Sirtuin 3/genetics ; Sirtuin 3/metabolism
Chemical Substances	Biomarkers ; DNA, Mitochondrial ; Asbestos (1332-21-4) ; SIRT3 protein, human (EC 3.5.1.-) ; Sirtuin 3 (EC 3.5.1.-)
Language	English
Publishing date	2021-06-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22136856
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Article ; Online: Aging imparts cell-autonomous dysfunction to regulatory T cells during recovery from influenza pneumonia.

Morales-Nebreda, Luisa / Helmin, Kathryn A / Torres Acosta, Manuel A / Markov, Nikolay S / Hu, Jennifer Yuan-Shih / Joudi, Anthony M / Piseaux-Aillon, Raul / Abdala-Valencia, Hiam / Politanska, Yuliya / Singer, Benjamin D

JCI insight

2021 Volume 6, Issue 6

Abstract: Regulatory T (Treg) cells orchestrate resolution and repair of acute lung inflammation and injury after viral pneumonia. Compared with younger patients, older individuals experience impaired recovery and worse clinical outcomes after severe viral ... ...

Abstract	Regulatory T (Treg) cells orchestrate resolution and repair of acute lung inflammation and injury after viral pneumonia. Compared with younger patients, older individuals experience impaired recovery and worse clinical outcomes after severe viral infections, including influenza and SARS coronavirus 2 (SARS-CoV-2). Whether age is a key determinant of Treg cell prorepair function after lung injury remains unknown. Here, we showed that aging results in a cell-autonomous impairment of reparative Treg cell function after experimental influenza pneumonia. Transcriptional and DNA methylation profiling of sorted Treg cells provided insight into the mechanisms underlying their age-related dysfunction, with Treg cells from aged mice demonstrating both loss of reparative programs and gain of maladaptive programs. Strategies to restore youthful Treg cell functional programs could be leveraged as therapies to improve outcomes among older individuals with severe viral pneumonia.
MeSH term(s)	Age Factors ; Aging/metabolism ; Aging/physiology ; Animals ; COVID-19/complications ; COVID-19/metabolism ; COVID-19/pathology ; COVID-19/virology ; Humans ; Influenza A virus ; Influenza, Human/complications ; Influenza, Human/metabolism ; Influenza, Human/pathology ; Influenza, Human/virology ; Lung/metabolism ; Lung/pathology ; Mice, Inbred C57BL ; Pneumonia, Viral/etiology ; Pneumonia, Viral/metabolism ; Pneumonia, Viral/pathology ; Pneumonia, Viral/virology ; SARS-CoV-2 ; T-Lymphocytes, Regulatory/metabolism ; T-Lymphocytes, Regulatory/pathology ; Mice
Language	English
Publishing date	2021-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.141690
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Article ; Online: Mitochondria regulate proliferation in adult cardiac myocytes.

Waypa, Gregory B / Smith, Kimberly A / Mungai, Paul T / Dudley, Vincent J / Helmin, Kathryn A / Singer, Benjamin D / Peek, Clara Bien / Bass, Joseph / Beussink-Nelson, Lauren / Shah, Sanjiv J / Ofman, Gaston / Wasserstrom, J Andrew / Muller, William A / Misharin, Alexander V / Budinger, G R Scott / Abdala-Valencia, Hiam / Chandel, Navdeep S / Dokic, Danijela / Bartom, Elizabeth T /

Zhang, Shuang / Tatekoshi, Yuki / Mahmoodzadeh, Amir / Ardehali, Hossein / Thorp, Edward B / Schumacker, Paul T

The Journal of clinical investigation

2024

Abstract: Newborn mammalian cardiomyocytes quickly transition from a fetal to an adult phenotype that utilizes mitochondrial oxidative phosphorylation but loses mitotic capacity. We tested whether forced reversal of adult cardiomyocytes back to a fetal glycolytic ... ...

Abstract	Newborn mammalian cardiomyocytes quickly transition from a fetal to an adult phenotype that utilizes mitochondrial oxidative phosphorylation but loses mitotic capacity. We tested whether forced reversal of adult cardiomyocytes back to a fetal glycolytic phenotype would restore proliferative capacity. We deleted Uqcrfs1 (mitochondrial Rieske Iron-Sulfur protein, RISP) in hearts of adult mice. As RISP protein decreased, heart mitochondrial function declined, and glucose utilization increased. Simultaneously, they underwent hyperplastic remodeling during which cardiomyocyte number doubled without cellular hypertrophy. Cellular energy supply was preserved, AMPK activation was absent, and mTOR activation was evident. In ischemic hearts with RISP deletion, new cardiomyocytes migrated into the infarcted region, suggesting the potential for therapeutic cardiac regeneration. RNA-seq revealed upregulation of genes associated with cardiac development and proliferation. Metabolomic analysis revealed a decrease in alpha-ketoglutarate (required for TET-mediated demethylation) and an increase in S-adenosylmethionine (required for methyltransferase activity). Analysis revealed an increase in methylated CpGs near gene transcriptional start sites. Genes that were both differentially expressed and differentially methylated were linked to upregulated cardiac developmental pathways. We conclude that decreased mitochondrial function and increased glucose utilization can restore mitotic capacity in adult cardiomyocytes resulting in the generation of new heart cells, potentially through the modification of substrates that regulate epigenetic modification of genes required for proliferation.
Language	English
Publishing date	2024-05-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI165482
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