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Article ; Online: Nuclear ADP-ribosylation drives IFNγ-dependent STAT1α enhancer formation in macrophages.

Gupte, Rebecca / Nandu, Tulip / Kraus, W Lee

2021 Volume 12, Issue 1, Page(s) 3931

Abstract: STAT1α is a key transcription factor driving pro-inflammatory responses in macrophages. We found that the interferon gamma (IFNγ)-regulated transcriptional program in macrophages is controlled by ADP-ribosylation (ADPRylation) of STAT1α, a post- ... ...

Abstract	STAT1α is a key transcription factor driving pro-inflammatory responses in macrophages. We found that the interferon gamma (IFNγ)-regulated transcriptional program in macrophages is controlled by ADP-ribosylation (ADPRylation) of STAT1α, a post-translational modification resulting in the site-specific covalent attachment of ADP-ribose moieties. PARP-1, the major nuclear poly(ADP-ribose) polymerase (PARP), supports IFNγ-stimulated enhancer formation by regulating the genome-wide binding and IFNγ-dependent transcriptional activation of STAT1α. It does so by ADPRylating STAT1α on specific residues in its DNA-binding domain (DBD) and transcription activation (TA) domain. ADPRylation of the DBD controls STAT1α binding to its cognate DNA elements, whereas ADPRylation of the TA domain regulates enhancer activation by modulating STAT1α phosphorylation and p300 acetyltransferase activity. Loss of ADPRylation at either site leads to diminished IFNγ-dependent transcription and downstream pro-inflammatory responses. We conclude that PARP-1-mediated ADPRylation of STAT1α drives distinct enhancer activation mechanisms and is a critical regulator of inflammatory responses in macrophages.
MeSH term(s)	ADP-Ribosylation ; Animals ; Binding Sites ; DNA/metabolism ; Enhancer Elements, Genetic ; Female ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Interferon-gamma/metabolism ; Macrophages/pathology ; Macrophages/physiology ; Male ; Mice, Inbred C57BL ; Phosphorylation ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly (ADP-Ribose) Polymerase-1/metabolism ; STAT1 Transcription Factor/chemistry ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; Transcriptional Activation ; Mice
Chemical Substances	STAT1 Transcription Factor ; Stat1 protein, mouse ; Interferon-gamma (82115-62-6) ; DNA (9007-49-2) ; Parp1 protein, mouse (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
Language	English
Publishing date	2021-06-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-24225-2
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Article ; Online: Nuclear ADP-ribosylation drives IFNγ-dependent STAT1α enhancer formation in macrophages

Rebecca Gupte / Tulip Nandu / W. Lee Kraus

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 18

Abstract: STAT1a is required for pro-inflammatory responses in macrophages. Here the authors reveal that post-translational modification of STAT1a, ADPribosylation, plays a critical role in enhancer formation and activation, thus modulating IFNγ-stimulated ... ...

Abstract	STAT1a is required for pro-inflammatory responses in macrophages. Here the authors reveal that post-translational modification of STAT1a, ADPribosylation, plays a critical role in enhancer formation and activation, thus modulating IFNγ-stimulated inflammatory responses in macrophages.
Keywords	Science ; Q
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article: Gray squirrels consume anthropogenic food waste most often during winter.

Rimbach, Rebecca / Butler, Gabrielle / Gupte, Pratik R / Jäger, Jörg / Parker, Claire / Pontzer, Herman

Mammalian biology = Zeitschrift fur Saugetierkunde

2022 Volume 103, Issue 1, Page(s) 69–81

Abstract: Urban habitats provide wildlife with predictable, easily accessible and abundant food sources in the form of human food waste. Urban eastern gray squirrels (: Supplementary information: The online version contains supplementary material available at ... ...

Abstract	Urban habitats provide wildlife with predictable, easily accessible and abundant food sources in the form of human food waste. Urban eastern gray squirrels ( Supplementary information: The online version contains supplementary material available at 10.1007/s42991-022-00326-3.
Language	English
Publishing date	2022-11-04
Publishing country	Switzerland
Document type	Journal Article
ISSN	1616-5047
ISSN	1616-5047
DOI	10.1007/s42991-022-00326-3
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Article ; Online: Combinatorial Treatment with PARP-1 Inhibitors and Cisplatin Attenuates Cervical Cancer Growth through Fos-Driven Changes in Gene Expression.

Gupte, Rebecca / Lin, Ken Y / Nandu, Tulip / Lea, Jayanthi S / Kraus, W Lee

Molecular cancer research : MCR

2022 Volume 20, Issue 8, Page(s) 1183–1192

Abstract: Cervical cancer continues to be a significant cause of cancer-related deaths in women. The most common treatment for cervical cancer involves the use of the drug cisplatin in conjunction with other therapeutics. However, the development of cisplatin ... ...

Abstract	Cervical cancer continues to be a significant cause of cancer-related deaths in women. The most common treatment for cervical cancer involves the use of the drug cisplatin in conjunction with other therapeutics. However, the development of cisplatin resistance in patients can hinder the efficacy of these treatments, so alternatives are needed. In this study, we found that PARP inhibitors (PARPi) could attenuate the growth of cells representing cervical adenocarcinoma and cervical squamous cell carcinoma. Moreover, a combination of PARPi with cisplatin increased cisplatin-mediated cytotoxicity in cervical cancer cells. This was accompanied by a dramatic alteration of the transcriptome. The FOS gene, which encodes the transcription factor Fos, was one of the most highly upregulated genes in the dual treatment condition, leading to increased Fos protein levels, greater Fos binding to chromatin, and the subsequent induction of Fos target genes. Increased expression of Fos was sufficient to hinder cervical cancer growth, as shown by ectopic expression of Fos in cervical cancer cells. Conversely, Fos knockdown enhanced cell growth. Collectively, these results indicate that by inducing FOS expression, PARPi treatment in combination with cisplatin leads to inhibition of cervical cancer proliferation, likely through a Fos-specific gene expression program. Implications: Our observations, which link the gene regulatory effects of PARPi + cisplatin to the growth inhibitory effects of FOS expression in cervical cancer cells, strengthen the rationale for using PARPi with cisplatin as a therapy for cervical cancer.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis ; Cisplatin/pharmacology ; Drug Resistance, Neoplasm ; Female ; Gene Expression ; Humans ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-fos/genetics ; Transcription Factors/genetics ; Uterine Cervical Neoplasms/drug therapy ; Uterine Cervical Neoplasms/genetics ; Uterine Cervical Neoplasms/pathology
Chemical Substances	Antineoplastic Agents ; FOS protein, human ; Poly(ADP-ribose) Polymerase Inhibitors ; Proto-Oncogene Proteins c-fos ; Transcription Factors ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2022-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-22-0111
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Article ; Online: PARPs in lipid metabolism and related diseases.

Szántó, Magdolna / Gupte, Rebecca / Kraus, W Lee / Pacher, Pal / Bai, Peter

Progress in lipid research

2021 Volume 84, Page(s) 101117

Abstract: PARPs and tankyrases (TNKS) represent a family of 17 proteins. PARPs and tankyrases were originally identified as DNA repair factors, nevertheless, recent advances have shed light on their role in lipid metabolism. To date, PARP1, PARP2, PARP3, ... ...

Abstract	PARPs and tankyrases (TNKS) represent a family of 17 proteins. PARPs and tankyrases were originally identified as DNA repair factors, nevertheless, recent advances have shed light on their role in lipid metabolism. To date, PARP1, PARP2, PARP3, tankyrases, PARP9, PARP10, PARP14 were reported to have multi-pronged connections to lipid metabolism. The activity of PARP enzymes is fine-tuned by a set of cholesterol-based compounds as oxidized cholesterol derivatives, steroid hormones or bile acids. In turn, PARPs modulate several key processes of lipid homeostasis (lipotoxicity, fatty acid and steroid biosynthesis, lipoprotein homeostasis, fatty acid oxidation, etc.). PARPs are also cofactors of lipid-responsive nuclear receptors and transcription factors through which PARPs regulate lipid metabolism and lipid homeostasis. PARP activation often represents a disruptive signal to (lipid) metabolism, and PARP-dependent changes to lipid metabolism have pathophysiological role in the development of hyperlipidemia, obesity, alcoholic and non-alcoholic fatty liver disease, type II diabetes and its complications, atherosclerosis, cardiovascular aging and skin pathologies, just to name a few. In this synopsis we will review the evidence supporting the beneficial effects of pharmacological PARP inhibitors in these diseases/pathologies and propose repurposing PARP inhibitors already available for the treatment of various malignancies.
MeSH term(s)	Cholesterol ; Diabetes Mellitus, Type 2 ; Fatty Acids ; Humans ; Lipid Metabolism ; Non-alcoholic Fatty Liver Disease ; Poly(ADP-ribose) Polymerases ; Proto-Oncogene Proteins
Chemical Substances	Fatty Acids ; Proto-Oncogene Proteins ; Cholesterol (97C5T2UQ7J) ; PARP10 protein, human (EC 2.4.2.30) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
Language	English
Publishing date	2021-08-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	282560-0
ISSN	1873-2194 ; 0079-6832 ; 0163-7827
ISSN (online)	1873-2194
ISSN	0079-6832 ; 0163-7827
DOI	10.1016/j.plipres.2021.101117
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Article ; Online: PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes.

Gupte, Rebecca / Liu, Ziying / Kraus, W Lee

Genes & development

2017 Volume 31, Issue 2, Page(s) 101–126

Abstract: The discovery of poly(ADP-ribose) >50 years ago opened a new field, leading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and the ADP-ribosylation reactions that they catalyze. Although the field was initially ... ...

Abstract	The discovery of poly(ADP-ribose) >50 years ago opened a new field, leading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and the ADP-ribosylation reactions that they catalyze. Although the field was initially focused primarily on the biochemistry and molecular biology of PARP-1 in DNA damage detection and repair, the mechanistic and functional understanding of the role of PARPs in different biological processes has grown considerably of late. This has been accompanied by a shift of focus from enzymology to a search for substrates as well as the first attempts to determine the functional consequences of site-specific ADP-ribosylation on those substrates. Supporting these advances is a host of methodological approaches from chemical biology, proteomics, genomics, cell biology, and genetics that have propelled new discoveries in the field. New findings on the diverse roles of PARPs in chromatin regulation, transcription, RNA biology, and DNA repair have been complemented by recent advances that link ADP-ribosylation to stress responses, metabolism, viral infections, and cancer. These studies have begun to reveal the promising ways in which PARPs may be targeted therapeutically for the treatment of disease. In this review, we discuss these topics and relate them to the future directions of the field.
MeSH term(s)	Animals ; DNA Repair/genetics ; Enzyme Activation ; Host-Pathogen Interactions ; Humans ; Molecular Biology/trends ; Nicotinamide-Nucleotide Adenylyltransferase/metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Signal Transduction/genetics ; Transcription, Genetic/genetics
Chemical Substances	Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Nicotinamide-Nucleotide Adenylyltransferase (EC 2.7.7.1)
Language	English
Publishing date	2017-01-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.291518.116
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Zs.A 2292: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Blockade of 20-hydroxyeicosatetraenoic acid receptor lowers blood pressure and alters vascular function in mice with smooth muscle-specific overexpression of CYP4A12-20-HETE synthase.

Agostinucci, Kevin / Hutcheson, Rebecca / Hossain, Sakib / Pascale, Jonathan V / Villegas, Elizabeth / Zhang, Frank / Adebesin, Adeniyi Michael / Falck, John R / Gupte, Sachin / Garcia, Victor / Schwartzman, Michal Laniado

Journal of hypertension

2022 Volume 40, Issue 3, Page(s) 498–511

Abstract: Objective: 20-Hydroxyeicosatetraenoic acid (20-HETE) is a vasoactive eicosanoid exhibiting effects on vascular smooth muscle cell (VSMC) via G-protein coupled receptor 75 (GPR75) and include stimulation of contractility, migration, and growth. We ... ...

Abstract	Objective: 20-Hydroxyeicosatetraenoic acid (20-HETE) is a vasoactive eicosanoid exhibiting effects on vascular smooth muscle cell (VSMC) via G-protein coupled receptor 75 (GPR75) and include stimulation of contractility, migration, and growth. We examined whether VSMC-targeted overexpression of CYP4A12, the primary 20-HETE-producing enzyme in mice, is sufficient to promote hypertension. Methods: Mice with VSM-specific Cyp4a12 overexpression (Myh11-4a12) and their littermate controls (WT) were generated by crossbreeding Cyp4a12-floxed with Myh11-Cre mice. The 20-HETE receptor blocker, N-disodium succinate-20-hydroxyeicosa-6(Z),15(Z)-diencarboxamide (AAA), was administered in the drinking water. Experiments were carried out for 12 days. SBP was measured by tail cuff. Renal interlobar and mesenteric arteries were harvested for assessment of gene expression, 20-HETE levels, vascular contractility, vasodilation, and remodeling. Results: Vascular and circulatory levels of 20-HETE were several folds higher in Myh11-4a12 mice compared with WT. The Myh11-4a12 mice compared with WT were hypertensive (145 ± 2 vs. 127 ± 2 mmHg; P < 0.05) and their vasculature displayed a contractile phenotype exemplified by increased contractility, reduced vasodilatory capacity, and increased media to lumen ratio. All these features were reversed by the administration of AAA. The mechanism of increased contractility includes, at least in part, Rho-kinase activation followed by increased myosin light chain phosphorylation and activation of the contractile apparatus. Conclusion: VSM-specific Cyp4a12 overexpression is sufficient to alter VSM cell phenotype through changes in contractile markers and enhancement in contractility that promote hypertension and vascular dysfunction in a 20-HETE-dependent manner. The 20-HETE receptor GPR75 may represent a novel target for the treatment of hypertension and associated vascular conditions.
MeSH term(s)	Animals ; Blood Pressure ; Humans ; Hydroxyeicosatetraenoic Acids/metabolism ; Hypertension ; Mice ; Muscle, Smooth/metabolism ; Receptors, G-Protein-Coupled
Chemical Substances	GPR75 protein, human ; Hydroxyeicosatetraenoic Acids ; Receptors, G-Protein-Coupled ; 20-hydroxy-5,8,11,14-eicosatetraenoic acid (79551-86-3)
Language	English
Publishing date	2022-01-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0000000000003038
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Article ; Online: Nuclear receptors in inflammation control: repression by GR and beyond.

Chinenov, Yurii / Gupte, Rebecca / Rogatsky, Inez

Molecular and cellular endocrinology

2013 Volume 380, Issue 1-2, Page(s) 55–64

Abstract: Inflammation is a protective response of organisms to pathogens, irritation or injury. Primary inflammatory sensors activate an array of signaling pathways that ultimately converge upon a few transcription factors such as AP1, NFκB and STATs that in turn ...

Abstract	Inflammation is a protective response of organisms to pathogens, irritation or injury. Primary inflammatory sensors activate an array of signaling pathways that ultimately converge upon a few transcription factors such as AP1, NFκB and STATs that in turn stimulate expression of inflammatory genes to ultimately eradicate infection and repair the damage. A disturbed balance between activation and inhibition of inflammatory pathways can set the stage for chronic inflammation which is increasingly recognized as a key pathogenic component of autoimmune, metabolic, cardiovascular and neurodegenerative disorders. Nuclear receptors (NRs) are a large family of transcription factors many of which are known for their potent anti-inflammatory actions. Activated by small lipophilic ligands, NRs interact with a wide range of transcription factors, cofactors and chromatin-modifying enzymes, assembling numerous cell- and tissue-specific DNA-protein transcriptional regulatory complexes with diverse activities. Here we discuss established and emerging roles and mechanisms by which NRs and, in particular, the glucocorticoid receptor (GR) repress genes encoding cytokines, chemokines and other pro-inflammatory mediators.
MeSH term(s)	Animals ; Base Sequence ; Binding Sites ; Chemokines/genetics ; Chemokines/metabolism ; Consensus Sequence ; Epigenesis, Genetic ; Glucocorticoids/physiology ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Protein Binding ; Receptors, Cytoplasmic and Nuclear/physiology ; Receptors, Glucocorticoid/physiology ; Transcription, Genetic
Chemical Substances	Chemokines ; Glucocorticoids ; Receptors, Cytoplasmic and Nuclear ; Receptors, Glucocorticoid
Language	English
Publishing date	2013-04-26
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2013.04.006
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Article ; Online: Glucocorticoid receptor coordinates transcription factor-dominated regulatory network in macrophages.

Chinenov, Yurii / Coppo, Maddalena / Gupte, Rebecca / Sacta, Maria A / Rogatsky, Inez

BMC genomics

2014 Volume 15, Page(s) 656

Abstract: Background: Inflammation triggered by infection or injury is tightly controlled by glucocorticoid hormones which signal via a dedicated transcription factor, the Glucocorticoid Receptor (GR), to regulate hundreds of genes. However, the hierarchy of ... ...

Abstract	Background: Inflammation triggered by infection or injury is tightly controlled by glucocorticoid hormones which signal via a dedicated transcription factor, the Glucocorticoid Receptor (GR), to regulate hundreds of genes. However, the hierarchy of transcriptional responses to GR activation and the molecular basis of their oftentimes non-linear dynamics are not understood. Results: We investigated early glucocorticoid-driven transcriptional events in macrophages, a cell type highly responsive to both pro- and anti-inflammatory stimuli. Using whole transcriptome analyses in resting and acutely lipopolysaccharide (LPS)-stimulated macrophages, we show that early GR target genes form dense networks with the majority of control nodes represented by transcription factors. The expression dynamics of several glucocorticoid-responsive genes are consistent with feed forward loops (FFL) and coincide with rapid GR recruitment. Notably, GR binding sites in genes encoding members of the KLF transcription factor family colocalize with KLF binding sites. Moreover, our gene expression, transcription factor binding and computational data are consistent with the existence of the GR-KLF9-KLF2 incoherent FFL. Analysis of LPS-downregulated genes revealed striking enrichment in multimerized Zn-fingers- and KRAB domain-containing proteins known to bind nucleic acids and repress transcription by propagating heterochromatin. This raises an intriguing possibility that an increase in chromatin accessibility in inflammatory macrophages results from broad downregulation of negative chromatin remodelers. Conclusions: Pro- and anti-inflammatory stimuli alter the expression of a vast array of transcription factors and chromatin remodelers. By regulating multiple transcription factors, which propagate the initial hormonal signal, GR acts as a coordinating hub in anti-inflammatory responses. As several KLFs promote the anti-inflammatory program in macrophages, we propose that GR and KLFs functionally cooperate to curb inflammation.
MeSH term(s)	Animals ; Computational Biology ; Dexamethasone/pharmacology ; Down-Regulation/drug effects ; Gene Expression Profiling ; Gene Regulatory Networks/drug effects ; Glucocorticoids/pharmacology ; Kinetics ; Lipopolysaccharides/pharmacology ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/metabolism ; Mice ; Models, Biological ; Receptors, Glucocorticoid/metabolism ; Signal Transduction/drug effects ; Transcription Factors/metabolism ; Transcriptional Activation/drug effects
Chemical Substances	Glucocorticoids ; Lipopolysaccharides ; Receptors, Glucocorticoid ; Transcription Factors ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2014-08-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1471-2164
ISSN (online)	1471-2164
DOI	10.1186/1471-2164-15-656
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Article: Nuclear receptors in inflammation control: Repression by GR and beyond

Chinenov, Yurii / Gupte, Rebecca / Rogatsky, Inez

Molecular and cellular endocrinology. 2013 Nov. 5, v. 380, no. 1-2

2013

Abstract	Inflammation is a protective response of organisms to pathogens, irritation or injury. Primary inflammatory sensors activate an array of signaling pathways that ultimately converge upon a few transcription factors such as AP1, NFκB and STATs that in turn stimulate expression of inflammatory genes to ultimately eradicate infection and repair the damage. A disturbed balance between activation and inhibition of inflammatory pathways can set the stage for chronic inflammation which is increasingly recognized as a key pathogenic component of autoimmune, metabolic, cardiovascular and neurodegenerative disorders. Nuclear receptors (NRs) are a large family of transcription factors many of which are known for their potent anti-inflammatory actions. Activated by small lipophilic ligands, NRs interact with a wide range of transcription factors, cofactors and chromatin-modifying enzymes, assembling numerous cell- and tissue-specific DNA–protein transcriptional regulatory complexes with diverse activities. Here we discuss established and emerging roles and mechanisms by which NRs and, in particular, the glucocorticoid receptor (GR) repress genes encoding cytokines, chemokines and other pro-inflammatory mediators.
Keywords	anti-inflammatory activity ; chemokines ; enzymes ; genes ; glucocorticoid receptors ; inflammation ; neurodegenerative diseases ; pathogens ; signal transduction ; transcription (genetics) ; transcription factor NF-kappa B
Language	English
Dates of publication	2013-1105
Size	p. 55-64.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2013.04.006
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