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Article ; Online: Immunoprecipitation of DNA:RNA Hybrids Using the S9.6 Antibody.

Gibbons, Hunter R / Aune, Thomas M

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2161, Page(s) 195–207

Abstract: Formation of DNA:RNA hybrids or R-loops contributes to numerous biologic processes. The development of the S9.6 antibody makes the analysis of R-Loops (DNA:RNA hybrids) possible through immunoprecipitation. Here, we describe the isolation of DNA:RNA ... ...

Abstract	Formation of DNA:RNA hybrids or R-loops contributes to numerous biologic processes. The development of the S9.6 antibody makes the analysis of R-Loops (DNA:RNA hybrids) possible through immunoprecipitation. Here, we describe the isolation of DNA:RNA hybrid structures using the S9.6 antibody. Using this protocol, both the DNA and RNA binding partners of the R-loop can be analyzed via qPCR, whole genome sequencing, or other methods.
MeSH term(s)	Antibodies/immunology ; DNA/chemistry ; HEK293 Cells ; Humans ; Immunoprecipitation/methods ; R-Loop Structures/immunology ; RNA/chemistry ; Sequence Analysis, RNA/methods
Chemical Substances	Antibodies ; RNA (63231-63-0) ; DNA (9007-49-2)
Language	English
Publishing date	2020-07-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0680-3_14
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Article ; Online: Cell Type-Specific Induction of Inflammation-Associated Genes in Crohn's Disease and Colorectal Cancer.

Saul, Dominik / Leite Barros, Luísa / Wixom, Alexander Q / Gellhaus, Benjamin / Gibbons, Hunter R / Faubion, William A / Kosinsky, Robyn Laura

International journal of molecular sciences

2022 Volume 23, Issue 6

Abstract: Based on the rapid increase in incidence of inflammatory bowel disease (IBD), the identification of susceptibility genes and cell populations contributing to this condition is essential. Previous studies suggested multiple genes associated with the ... ...

Abstract	Based on the rapid increase in incidence of inflammatory bowel disease (IBD), the identification of susceptibility genes and cell populations contributing to this condition is essential. Previous studies suggested multiple genes associated with the susceptibility of IBD; however, due to the analysis of whole-tissue samples, the contribution of individual cell populations remains widely unresolved. Single-cell RNA sequencing (scRNA-seq) provides the opportunity to identify underlying cellular populations. We determined the enrichment of Crohn's disease (CD)-induced genes in a publicly available Crohn's disease scRNA-seq dataset and detected the strongest induction of these genes in innate lymphoid cells (ILC1), highly activated T cells and dendritic cells, pericytes and activated fibroblasts, as well as epithelial cells. Notably, these genes were highly enriched in IBD-associated neoplasia, as well as sporadic colorectal cancer (CRC). Indeed, the same six cell populations displayed an upregulation of CD-induced genes in a CRC scRNA-seq dataset. Finally, after integrating and harmonizing the CD and CRC scRNA-seq data, we demonstrated that these six cell types display a gradual increase in gene expression levels from a healthy state to an inflammatory and tumorous state. Together, we identified cell populations that specifically upregulate CD-induced genes in CD and CRC patients and could, therefore, contribute to inflammation-associated tumor development.
MeSH term(s)	Colitis, Ulcerative/pathology ; Colorectal Neoplasms/pathology ; Crohn Disease/pathology ; Humans ; Immunity, Innate ; Inflammation/complications ; Inflammation/genetics ; Inflammatory Bowel Diseases/pathology ; Lymphocytes/pathology
Language	English
Publishing date	2022-03-12
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/ijms23063082
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Article ; Online: The FOXP3

Kosinsky, Robyn Laura / Gonzalez, Michelle M / Saul, Dominik / Barros, Luísa Leite / Sagstetter, Mary R / Fedyshyn, Yaroslav / Nair, Asha / Sun, Zhifu / Hamdan, Feda H / Gibbons, Hunter R / Perez Pachon, Mauricio E / Druliner, Brooke R / Johnsen, Steven A / Faubion, William A

Gastroenterology

2024 Volume 166, Issue 4, Page(s) 631–644.e17

Abstract: Background & aims: The incidence of Crohn's disease (CD) continues to increase worldwide. The contribution of CD4: Methods: We performed single-cell RNA-sequencing in CD4: Results: We identified 5 distinct FOXP3: Conclusions: We identified a ... ...

Abstract	Background & aims: The incidence of Crohn's disease (CD) continues to increase worldwide. The contribution of CD4 Methods: We performed single-cell RNA-sequencing in CD4 Results: We identified 5 distinct FOXP3 Conclusions: We identified a novel, proinflammatory FOXP3
MeSH term(s)	Humans ; Crohn Disease/drug therapy ; Crohn Disease/genetics ; Crohn Disease/metabolism ; Vorinostat/metabolism ; T-Lymphocytes, Regulatory/metabolism ; Inflammation/metabolism ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism
Chemical Substances	Vorinostat (58IFB293JI) ; Forkhead Transcription Factors ; FOXP3 protein, human
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2024.01.007
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Article ; Online: Hypomethylation and Overexpression of Th17-Associated Genes is a Hallmark of Intestinal CD4+ Lymphocytes in Crohn's Disease.

Sun, Zhifu / Braga-Neto, Manuel B / Xiong, Yuning / Bhagwate, Adytia V / Gibbons, Hunter R / Sagstetter, Mary R / Hamdan, Feda H / Baheti, Saurabh / Friton, Jessica / Nair, Asha / Ye, Zhenqing / Faubion, William A

Journal of Crohn's & colitis

2023 Volume 17, Issue 11, Page(s) 1847–1857

Abstract: Background: The development of Crohn's disease [CD] involves immune cell signalling pathways regulated by epigenetic modifications. Aberrant DNA methylation has been identified in peripheral blood and bulk intestinal tissue from CD patients. However, ... ...

Abstract	Background: The development of Crohn's disease [CD] involves immune cell signalling pathways regulated by epigenetic modifications. Aberrant DNA methylation has been identified in peripheral blood and bulk intestinal tissue from CD patients. However, the DNA methylome of disease-associated intestinal CD4+ lymphocytes has not been evaluated. Materials and methods: Genome-wide DNA methylation sequencing was performed from terminal ileum CD4+ cells from 21 CD patients and 12 age- and sex-matched controls. Data were analysed for differentially methylated CpGs [DMCs] and methylated regions [DMRs]. Integration was performed with RNA-sequencing data to evaluate the functional impact of DNA methylation changes on gene expression. DMRs were overlapped with regions of differentially open chromatin [by ATAC-seq] and CCCTC-binding factor [CTCF] binding sites [by ChIP-seq] between peripherally derived Th17 and Treg cells. Results: CD4+ cells in CD patients had significantly increased DNA methylation compared to those from the controls. A total of 119 051 DMCs and 8113 DMRs were detected. While hypermethylated genes were mostly related to cell metabolism and homeostasis, hypomethylated genes were significantly enriched within the Th17 signalling pathway. The differentially enriched ATAC regions in Th17 cells [compared to Tregs] were hypomethylated in CD patients, suggesting heightened Th17 activity. There was significant overlap between hypomethylated DNA regions and CTCF-associated binding sites. Conclusions: The methylome of CD patients shows an overall dominant hypermethylation yet hypomethylation is more concentrated in proinflammatory pathways, including Th17 differentiation. Hypomethylation of Th17-related genes associated with areas of open chromatin and CTCF binding sites constitutes a hallmark of CD-associated intestinal CD4+ cells.
MeSH term(s)	Humans ; DNA Methylation ; Crohn Disease/genetics ; Crohn Disease/metabolism ; Th17 Cells ; CD4-Positive T-Lymphocytes/metabolism ; Chromatin/metabolism
Chemical Substances	Chromatin
Language	English
Publishing date	2023-07-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2390120-2
ISSN	1876-4479 ; 1873-9946
ISSN (online)	1876-4479
ISSN	1873-9946
DOI	10.1093/ecco-jcc/jjad093
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Article ; Online: Divergent lncRNA

Gibbons, Hunter R / Shaginurova, Guzel / Kim, Laura C / Chapman, Nathaniel / Spurlock, Charles F / Aune, Thomas M

Frontiers in immunology

2018 Volume 9, Page(s) 2512

Abstract: Long non-coding RNAs (lncRNAs) possess a diverse array of regulatory functions including activation and silencing of gene transcription, regulation of splicing, and coordinating epigenetic modifications. ...

Abstract	Long non-coding RNAs (lncRNAs) possess a diverse array of regulatory functions including activation and silencing of gene transcription, regulation of splicing, and coordinating epigenetic modifications.
MeSH term(s)	Cell Differentiation/genetics ; Cell Line ; Chromatin/genetics ; Cytokines/genetics ; Epigenesis, Genetic/genetics ; GATA3 Transcription Factor/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; RNA, Long Noncoding/genetics ; Th2 Cells ; Transcription, Genetic/genetics
Chemical Substances	Chromatin ; Cytokines ; GATA3 Transcription Factor ; GATA3 protein, human ; RNA, Long Noncoding
Language	English
Publishing date	2018-10-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.02512
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Article ; Online: Bromodomain inhibitor JQ1 reversibly blocks IFN-γ production.

Gibbons, Hunter R / Mi, Deborah J / Farley, Virginia M / Esmond, Tashawna / Kaood, Mary B / Aune, Thomas M

Scientific reports

2019 Volume 9, Issue 1, Page(s) 10280

Abstract: As a class, 'BET' inhibitors disrupt binding of bromodomain and extra-terminal motif (BET) proteins, BRD2, BRD3, BRD4 and BRDT, to acetylated histones preventing recruitment of RNA polymerase 2 to enhancers and promoters, especially super-enhancers, to ... ...

Abstract	As a class, 'BET' inhibitors disrupt binding of bromodomain and extra-terminal motif (BET) proteins, BRD2, BRD3, BRD4 and BRDT, to acetylated histones preventing recruitment of RNA polymerase 2 to enhancers and promoters, especially super-enhancers, to inhibit gene transcription. As such, BET inhibitors may be useful therapeutics for treatment of cancer and inflammatory disease. For example, the small molecule BET inhibitor, JQ1, selectively represses MYC, an important oncogene regulated by a super-enhancer. IFN-γ, a critical cytokine for both innate and adaptive immune responses, is also regulated by a super-enhancer. Here, we show that JQ1 represses IFN-γ expression in TH1 polarized PBMC cultures, CD4+ memory T cells, and NK cells. JQ1 treatment does not reduce activating chromatin marks at the IFNG locus, but displaces RNA polymerase II from the locus. Further, IFN-γ expression recovers in polarized TH1 cultures following removal of JQ1. Our results show that JQ1 abrogates IFN-γ expression, but repression is reversible. Thus, BET inhibitors may disrupt the normal functions of the innate and adaptive immune response.
MeSH term(s)	Adult ; Azepines/pharmacology ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Down-Regulation ; Humans ; Interferon-gamma/genetics ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/immunology ; Leukocytes, Mononuclear/cytology ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/metabolism ; RNA Polymerase II/metabolism ; Th1 Cells/drug effects ; Th1 Cells/immunology ; Triazoles/pharmacology
Chemical Substances	(+)-JQ1 compound ; Azepines ; IFNG protein, human ; Triazoles ; Interferon-gamma (82115-62-6) ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2019-07-16
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/s41598-019-46516-x
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Article ; Online: Long non-coding RNA ACTA2-AS1 promotes ductular reaction by interacting with the p300/ELK1 complex.

Navarro-Corcuera, Amaia / Sehrawat, Tejasav S / Jalan-Sakrikar, Nidhi / Gibbons, Hunter R / Pirius, Nicholas E / Khanal, Shalil / Hamdan, Feda H / Aseem, Sayed Obaidullah / Cao, Sheng / Banales, Jesus M / Kang, Ningling / Faubion, William A / LaRusso, Nicholas F / Shah, Vijay H / Huebert, Robert C

Journal of hepatology

2021 Volume 76, Issue 4, Page(s) 921–933

Abstract: Background & aims: Biliary disease is associated with a proliferative/fibrogenic ductular reaction (DR). p300 is an epigenetic regulator that acetylates lysine 27 on histone 3 (H3K27ac) and is activated during fibrosis. Long non-coding RNAs (lncRNAs) ... ...

Abstract	Background & aims: Biliary disease is associated with a proliferative/fibrogenic ductular reaction (DR). p300 is an epigenetic regulator that acetylates lysine 27 on histone 3 (H3K27ac) and is activated during fibrosis. Long non-coding RNAs (lncRNAs) are aberrantly expressed in cholangiopathies, but little is known about how they recruit epigenetic complexes and regulate DR. We investigated epigenetic complexes, including transcription factors (TFs) and lncRNAs, contributing to p300-mediated transcription during fibrosis. Methods: We evaluated p300 in vivo using tamoxifen-inducible, cholangiocyte-selective, p300 knockout (KO) coupled with bile duct ligation (BDL) and Mdr KO mice treated with SGC-CBP30. Primary cholangiocytes and liver tissue were analyzed for expression of Acta2-as1 lncRNA by qPCR and RNA in situ hybridization. In vitro, we performed RNA-sequencing in human cholangiocytes with a p300 inhibitor. Cholangiocytes were exposed to lipopolysaccharide (LPS) as an injury model. We confirmed formation of a p300/ELK1 complex by immunoprecipitation (IP). RNA IP was used to examine interactions between ACTA2-AS1 and p300. Chromatin IP assays were used to evaluate p300/ELK1 occupancy and p300-mediated H3K27ac. Organoids were generated from ACTA2-AS1-depleted cholangiocytes. Results: BDL-induced DR and fibrosis were reduced in Krt19-Cre Conclusion: Cholangiocyte-selective p300 KO or p300 inhibition attenuate DR/fibrosis in mice. ACTA2-AS1 influences recruitment of p300/ELK1 to specific promoters to drive H3K27ac and epigenetic activation of proliferative/fibrogenic genes. This suggests that cooperation between epigenetic co-activators and lncRNAs facilitates DR/fibrosis in biliary diseases. Lay summary: We identified a three-part complex containing an RNA molecule, a transcription factor, and an epigenetic enzyme. The complex is active in injured bile duct cells and contributes to activation of genes involved in proliferation and fibrosis.
MeSH term(s)	Animals ; Bile Ducts/pathology ; Cell Proliferation ; Fibrosis ; Lipopolysaccharides ; Liver/pathology ; Mice ; Mice, Knockout ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
Chemical Substances	Lipopolysaccharides ; RNA, Long Noncoding
Language	English
Publishing date	2021-12-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2021.12.014
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Article ; Online: BMI1 maintains the Treg epigenomic landscape to prevent inflammatory bowel disease.

Gonzalez, Michelle M / Bamidele, Adebowale O / Svingen, Phyllis A / Sagstetter, Mary R / Smyrk, Thomas C / Gaballa, Joseph M / Hamdan, Feda H / Kosinsky, Robyn Laura / Gibbons, Hunter R / Sun, Zhifu / Ye, Zhenqing / Nair, Asha / Ramos, Guilherme P / Braga Neto, Manuel B / Wixom, Alexander Q / Mathison, Angela J / Johnsen, Steven A / Urrutia, Raul / Faubion, William A

The Journal of clinical investigation

2021 Volume 131, Issue 12

Abstract: FOXP3+ Tregs are expanded within the inflamed intestine of human Crohn's disease, yet FOXP3-mediated gene repression within these cells is lost. The polycomb repressive complexes play a role in FOXP3 target gene regulation, but deeper mechanistic insight ...

Abstract	FOXP3+ Tregs are expanded within the inflamed intestine of human Crohn's disease, yet FOXP3-mediated gene repression within these cells is lost. The polycomb repressive complexes play a role in FOXP3 target gene regulation, but deeper mechanistic insight is incomplete. We have now specifically identified the polycomb-repressive complex 1 (PRC1) family member, BMI1 in the regulation of a proinflammatory enhancer network in both human and murine Tregs. Using human Tregs and lamina propria T cells, we inferred PRC1 to regulate Crohn's associated gene networks through assays of chromatin accessibility. Conditional deletion of BMI1 in murine FOXP3+ cells led to systemic inflammation. BMI1-deficient Tregs beared a TH1/TH17-like phenotype as assessed by assays of genome wide transcription, chromatin accessibility and proteomic techniques. Finally, BMI1 mutant FOXP3+ cells did not suppress colitis in the adoptive transfer model of human inflammatory bowel disease. We propose that BMI1 plays an important role in enforcing Treg identity in vitro and in vivo. Loss of Treg identity via genetic or transient BMI1 depletion perturbs the epigenome and converts Tregs into Th1/Th17-like proinflammatory cells, a transition relevant to human Crohn's disease associated CD4+ T cells.
MeSH term(s)	Animals ; Crohn Disease/genetics ; Crohn Disease/immunology ; Epigenesis, Genetic/immunology ; Humans ; Mice ; Mice, Transgenic ; Polycomb Repressive Complex 1/genetics ; Polycomb Repressive Complex 1/immunology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/pathology ; Th1 Cells/immunology ; Th17 Cells/immunology
Chemical Substances	Bmi1 protein, mouse ; Proto-Oncogene Proteins ; Polycomb Repressive Complex 1 (EC 2.3.2.27)
Language	English
Publishing date	2021-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI140755
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Article ; Online: G9a Modulates Lipid Metabolism in CD4 T Cells to Regulate Intestinal Inflammation.

Ramos, Guilherme Piovezani / Bamidele, Adebowale O / Klatt, Emily E / Sagstetter, Mary R / Kurdi, Ahmed T / Hamdan, Feda H / Kosinsky, Robyn Laura / Gaballa, Joseph M / Nair, Asha / Sun, Zhifu / Dasari, Surendra / Lanza, Ian R / Rozeveld, Cody N / Schott, Micah B / Urrutia, Guillermo / Westphal, Maria S / Clarkson, Benjamin D / Howe, Charles L / Marietta, Eric V /

Luckey, David H / Murray, Joseph A / Gonzalez, Michelle / Braga Neto, Manuel B / Gibbons, Hunter R / Smyrk, Thomas C / Johnsen, Steven / Lomberk, Gwen / Faubion, William A

Gastroenterology

2022 Volume 164, Issue 2, Page(s) 256–271.e10

Abstract: Background & aims: Although T-cell intrinsic expression of G9a has been associated with murine intestinal inflammation, mechanistic insight into the role of this methyltransferase in human T-cell differentiation is ill defined, and manipulation of G9a ... ...

Abstract	Background & aims: Although T-cell intrinsic expression of G9a has been associated with murine intestinal inflammation, mechanistic insight into the role of this methyltransferase in human T-cell differentiation is ill defined, and manipulation of G9a function for therapeutic use against inflammatory disorders is unexplored. Methods: Human naive T cells were isolated from peripheral blood and differentiated in vitro in the presence of a G9a inhibitor (UNC0642) before being characterized via the transcriptome (RNA sequencing), chromatin accessibility (assay for transposase-accessible chromatin by sequencing), protein expression (cytometry by time of flight, flow cytometry), metabolism (mitochondrial stress test, ultrahigh performance liquid chromatography-tandem mas spectroscopy) and function (T-cell suppression assay). The in vivo role of G9a was assessed using 3 murine models. Results: We discovered that pharmacologic inhibition of G9a enzymatic function in human CD4 T cells led to spontaneous generation of FOXP3 Conclusion: G9a inhibition promotes cholesterol metabolism in T cells, favoring a metabolic profile that facilitates Treg development in vitro and in vivo. Our data support the potential use of G9a inhibitors in the treatment of immune-mediated conditions including inflammatory bowel disease.
MeSH term(s)	Mice ; Humans ; Animals ; CD4-Positive T-Lymphocytes ; Lipid Metabolism ; T-Lymphocytes, Regulatory/metabolism ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/genetics ; Chromatin ; Inflammation ; Cholesterol ; Lipids ; Forkhead Transcription Factors/metabolism
Chemical Substances	Chromatin ; Cholesterol (97C5T2UQ7J) ; Lipids ; Forkhead Transcription Factors
Language	English
Publishing date	2022-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2022.10.011
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