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Article ; Online: Letting off electrons to cope with metabolic stress.

Heer, Collin D / Brenner, Charles

Nature metabolism

2020 Volume 2, Issue 6, Page(s) 485–486

Language	English
Publishing date	2020-07-21
Publishing country	Germany
Document type	Journal Article
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-020-0207-8
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Article ; Online: Identification of (

He, Yingfang / Krämer, Stefanie D / Grether, Uwe / Wittwer, Matthias B / Collin, Ludovic / Kuhn, Bernd / Topp, Andreas / Heer, Dominik / O'Hara, Fionn / Honer, Michael / Pavlovic, Anto / Richter, Hans / Ritter, Martin / Rombach, Didier / Keller, Claudia / Gobbi, Luca / Mu, Linjing

Journal of nuclear medicine : official publication, Society of Nuclear Medicine

2024 Volume 65, Issue 2, Page(s) 300–305

Abstract: This study aimed to evaluate ( ...

Abstract	This study aimed to evaluate (
MeSH term(s)	Rats ; Mice ; Male ; Animals ; Monoacylglycerol Lipases/metabolism ; Rats, Wistar ; Neuroimaging/methods ; Brain/diagnostic imaging ; Brain/metabolism ; Positron-Emission Tomography/methods ; Mice, Knockout ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/chemistry
Chemical Substances	Monoacylglycerol Lipases (EC 3.1.1.23) ; Enzyme Inhibitors
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	80272-4
ISSN	1535-5667 ; 0097-9058 ; 0161-5505 ; 0022-3123
ISSN (online)	1535-5667
ISSN	0097-9058 ; 0161-5505 ; 0022-3123
DOI	10.2967/jnumed.123.266426
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Zs.A 114: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 328: Show issues

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Article ; Online: Succinate Accumulation Links Mitochondrial MnSOD Depletion to Aberrant Nuclear DNA Methylation and Altered Cell Fate.

Cramer-Morales, Kimberly L / Heer, Collin D / Mapuskar, Kranti A / Domann, Frederick E

Journal of Experimental Pathology

2020 Volume 1, Issue 2, Page(s) 60–70

Abstract: Previous studies showed that human cell line HEK293 lacking mitochondrial superoxide dismutase (MnSOD) exhibited decreased succinate dehydrogenase (SDH) activity, and mice lacking MnSOD displayed significant reductions in SDH and aconitase activities. ... ...

Abstract	Previous studies showed that human cell line HEK293 lacking mitochondrial superoxide dismutase (MnSOD) exhibited decreased succinate dehydrogenase (SDH) activity, and mice lacking MnSOD displayed significant reductions in SDH and aconitase activities. Since MnSOD has significant effects on SDH activity, and succinate is a key regulator of TET enzymes needed for proper differentiation, we hypothesized that
Language	English
Publishing date	2020-12-09
Publishing country	United States
Document type	Journal Article
ISSN	2694-5061
ISSN (online)	2694-5061
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Article ; Online: Preclinical Evaluation of the Reversible Monoacylglycerol Lipase PET Tracer (R)-[

He, Yingfang / Delparente, Aro / Jie, Caitlin V M L / Keller, Claudia / Humm, Roland / Heer, Dominik / Collin, Ludovic / Schibli, Roger / Gobbi, Luca / Grether, Uwe / Mu, Linjing

Chembiochem : a European journal of chemical biology

2024 Volume 25, Issue 7, Page(s) e202300819

Abstract: Monoacylglycerol lipase (MAGL) plays a crucial role in the degradation of 2-arachidonoylglycerol (2-AG), one of the major endocannabinoids in the brain. Inhibiting MAGL could lead to increased levels of 2-AG, which showed beneficial effects on pain ... ...

Abstract	Monoacylglycerol lipase (MAGL) plays a crucial role in the degradation of 2-arachidonoylglycerol (2-AG), one of the major endocannabinoids in the brain. Inhibiting MAGL could lead to increased levels of 2-AG, which showed beneficial effects on pain management, anxiety, inflammation, and neuroprotection. In the current study, we report the characterization of an enantiomerically pure (R)-[
MeSH term(s)	Rats ; Mice ; Animals ; Monoacylglycerol Lipases/metabolism ; Neurodegenerative Diseases/diagnostic imaging ; Neurodegenerative Diseases/drug therapy ; Positron-Emission Tomography/methods ; Inflammation ; Drug Development ; Enzyme Inhibitors/pharmacology
Chemical Substances	Monoacylglycerol Lipases (EC 3.1.1.23) ; Enzyme Inhibitors
Language	English
Publishing date	2024-03-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2020469-3
ISSN	1439-7633 ; 1439-4227
ISSN (online)	1439-7633
ISSN	1439-4227
DOI	10.1002/cbic.202300819
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Article ; Online: Multi-parameter optimization: Development of a morpholin-3-one derivative with an improved kinetic profile for imaging monoacylglycerol lipase in the brain.

European journal of medicinal chemistry

2022 Volume 243, Page(s) 114750

Abstract: Monoacylglycerol lipase (MAGL) is a gatekeeper in regulating endocannabinoid signaling and has gained substantial attention as a therapeutic target for neurological disorders. We recently discovered a morpholin-3-one derivative as a novel scaffold for ... ...

Abstract	Monoacylglycerol lipase (MAGL) is a gatekeeper in regulating endocannabinoid signaling and has gained substantial attention as a therapeutic target for neurological disorders. We recently discovered a morpholin-3-one derivative as a novel scaffold for imaging MAGL via positron emission tomography (PET). However, its slow kinetics in vivo hampered the application. In this study, structural optimization was conducted and eleven novel MAGL inhibitors were designed and synthesized. Based on the results from MAGL inhibitory potency, in vitro metabolic stability and surface plasmon resonance assays, we identified compound 7 as a potential MAGL PET tracer candidate. [
MeSH term(s)	Animals ; Mice ; Humans ; Monoacylglycerol Lipases/metabolism ; Tomography, X-Ray Computed ; Positron-Emission Tomography/methods ; Brain/metabolism ; Kinetics ; Enzyme Inhibitors/chemistry
Chemical Substances	Monoacylglycerol Lipases (EC 3.1.1.23) ; Enzyme Inhibitors
Language	English
Publishing date	2022-09-09
Publishing country	France
Document type	Journal Article
ZDB-ID	188597-2
ISSN	1768-3254 ; 0009-4374 ; 0223-5234
ISSN (online)	1768-3254
ISSN	0009-4374 ; 0223-5234
DOI	10.1016/j.ejmech.2022.114750
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Zs.B 784: Show issues

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Article ; Online: Inhibition of CD38 and supplementation of nicotinamide riboside ameliorate lipopolysaccharide-induced microglial and astrocytic neuroinflammation by increasing NAD

Roboon, Jureepon / Hattori, Tsuyoshi / Ishii, Hiroshi / Takarada-Iemata, Mika / Nguyen, Dinh Thi / Heer, Collin D / O'Meally, Denis / Brenner, Charles / Yamamoto, Yasuhiko / Okamoto, Hiroshi / Higashida, Haruhiro / Hori, Osamu

Journal of neurochemistry

2021 Volume 158, Issue 2, Page(s) 311–327

Abstract: Neuroinflammation is initiated by activation of the brain's innate immune system in response to an inflammatory challenge. Insufficient control of neuroinflammation leads to enhanced or prolonged pathology in various neurological conditions including ... ...

Abstract	Neuroinflammation is initiated by activation of the brain's innate immune system in response to an inflammatory challenge. Insufficient control of neuroinflammation leads to enhanced or prolonged pathology in various neurological conditions including multiple sclerosis and Alzheimer's disease. Nicotinamide adenine dinucleotide (NAD
MeSH term(s)	ADP-ribosyl Cyclase 1/antagonists & inhibitors ; Animals ; Apigenin/pharmacology ; Astrocytes/drug effects ; Astrocytes/pathology ; Chemokines/metabolism ; Cytokines/metabolism ; Gene Deletion ; Hippocampus/drug effects ; Hippocampus/metabolism ; Inflammation/chemically induced ; Inflammation/pathology ; Injections, Intraventricular ; Lipopolysaccharides/administration & dosage ; Macrophage Activation/drug effects ; Male ; Membrane Glycoproteins/antagonists & inhibitors ; Mice ; Mice, Inbred ICR ; Mice, Knockout ; Microglia/drug effects ; Microglia/pathology ; NAD/metabolism ; NAD/pharmacology ; NF-kappa B/genetics ; Nerve Degeneration ; Niacinamide/analogs & derivatives ; Niacinamide/pharmacology ; Pyridinium Compounds/pharmacology
Chemical Substances	Chemokines ; Cytokines ; Lipopolysaccharides ; Membrane Glycoproteins ; NF-kappa B ; Pyridinium Compounds ; nicotinamide-beta-riboside (0I8H2M0L7N) ; NAD (0U46U6E8UK) ; Niacinamide (25X51I8RD4) ; Apigenin (7V515PI7F6) ; Cd38 protein, mouse (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2021-05-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15367
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Ui II Zs.170: Show issues

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Article ; Online: Avasopasem manganese synergizes with hypofractionated radiation to ablate tumors through the generation of hydrogen peroxide.

Sishc, Brock J / Ding, Lianghao / Nam, Taek-Keun / Heer, Collin D / Rodman, Samuel N / Schoenfeld, Joshua D / Fath, Melissa A / Saha, Debabrata / Pulliam, Casey F / Langen, Britta / Beardsley, Robert A / Riley, Dennis P / Keene, Jeffery L / Spitz, Douglas R / Story, Michael D

Science translational medicine

2021 Volume 13, Issue 593

Abstract: Avasopasem manganese (AVA or GC4419), a selective superoxide dismutase mimetic, is in a phase 3 clinical trial (NCT03689712) as a mitigator of radiation-induced mucositis in head and neck cancer based on its superoxide scavenging activity. We tested ... ...

Abstract	Avasopasem manganese (AVA or GC4419), a selective superoxide dismutase mimetic, is in a phase 3 clinical trial (NCT03689712) as a mitigator of radiation-induced mucositis in head and neck cancer based on its superoxide scavenging activity. We tested whether AVA synergized with radiation via the generation of hydrogen peroxide, the product of superoxide dismutation, to target tumor cells in preclinical xenograft models of non-small cell lung cancer (NSCLC), head and neck squamous cell carcinoma, and pancreatic ductal adenocarcinoma. Treatment synergy with AVA and high dose per fraction radiation occurred when mice were given AVA once before tumor irradiation and further increased when AVA was given before and for 4 days after radiation, supporting a role for oxidative metabolism. This synergy was abrogated by conditional overexpression of catalase in the tumors. In addition, in vitro NSCLC and mammary adenocarcinoma models showed that AVA increased intracellular hydrogen peroxide concentrations and buthionine sulfoximine- and auranofin-induced inhibition of glutathione- and thioredoxin-dependent hydrogen peroxide metabolism selectively enhanced AVA-induced killing of cancer cells compared to normal cells. Gene expression in irradiated tumors treated with AVA suggested that increased inflammatory, TNFα, and apoptosis signaling also contributed to treatment synergy. These results support the hypothesis that AVA, although reducing radiotherapy damage to normal tissues, acts synergistically only with high dose per fraction radiation regimens analogous to stereotactic ablative body radiotherapy against tumors by a hydrogen peroxide-dependent mechanism. This tumoricidal synergy is now being tested in a phase I-II clinical trial in humans (NCT03340974).
MeSH term(s)	Animals ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Humans ; Hydrogen Peroxide ; Lung Neoplasms/drug therapy ; Lung Neoplasms/radiotherapy ; Mice ; Organometallic Compounds ; Superoxide Dismutase
Chemical Substances	Organometallic Compounds ; Hydrogen Peroxide (BBX060AN9V) ; Superoxide Dismutase (EC 1.15.1.1) ; avasopasem manganese (EY1WA413UL)
Language	English
Publishing date	2021-05-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abb3768
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Zs.A 6941: Show issues

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Article: Coronavirus infection and PARP expression dysregulate the NAD Metabolome: an actionable component of innate immunity.

Heer, Collin D / Sanderson, Daniel J / Voth, Lynden S / Alhammad, Yousef M O / Schmidt, Mark S / Trammell, Samuel A J / Perlman, Stanley / Cohen, Michael S / Fehr, Anthony R / Brenner, Charles

bioRxiv : the preprint server for biology

2020

Abstract: Poly-ADP-ribose polymerase (PARP) superfamily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using nicotinamide adenine dinucleotide (NAD) as the source of ADPR. While the well-known poly-ADP-ribosylating ( ... ...

Abstract	Poly-ADP-ribose polymerase (PARP) superfamily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using nicotinamide adenine dinucleotide (NAD) as the source of ADPR. While the well-known poly-ADP-ribosylating (PARylating) PARPs primarily function in the DNA damage response, many non-canonical mono-ADP-ribosylating (MARylating) PARPs are associated with cellular antiviral responses. We recently demonstrated robust upregulation of several PARPs following infection with Murine Hepatitis Virus (MHV), a model coronavirus. Here we show that SARS-CoV-2 infection strikingly upregulates MARylating PARPs and induces the expression of genes encoding enzymes for salvage NAD synthesis from nicotinamide (NAM) and nicotinamide riboside (NR), while downregulating other NAD biosynthetic pathways. We show that overexpression of PARP10 is sufficient to depress cellular NAD and that the activities of the transcriptionally induced enzymes PARP7, PARP10, PARP12 and PARP14 are limited by cellular NAD and can be enhanced by pharmacological activation of NAD synthesis. We further demonstrate that infection with MHV induces a severe attack on host cell NAD
Keywords	covid19
Language	English
Publishing date	2020-10-06
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.04.17.047480
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Article ; Online: Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity.

Heer, Collin D / Sanderson, Daniel J / Voth, Lynden S / Alhammad, Yousef M O / Schmidt, Mark S / Trammell, Samuel A J / Perlman, Stanley / Cohen, Michael S / Fehr, Anthony R / Brenner, Charles

The Journal of biological chemistry

2020 Volume 295, Issue 52, Page(s) 17986–17996

Abstract: Poly(ADP-ribose) polymerase (PARP) superfamily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using NAD as the source of ADPR. Although the well-known poly(ADP-ribosylating) (PARylating) PARPs primarily ... ...

Abstract	Poly(ADP-ribose) polymerase (PARP) superfamily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using NAD as the source of ADPR. Although the well-known poly(ADP-ribosylating) (PARylating) PARPs primarily function in the DNA damage response, many noncanonical mono(ADP-ribosylating) (MARylating) PARPs are associated with cellular antiviral responses. We recently demonstrated robust up-regulation of several PARPs following infection with murine hepatitis virus (MHV), a model coronavirus. Here we show that SARS-CoV-2 infection strikingly up-regulates MARylating PARPs and induces the expression of genes encoding enzymes for salvage NAD synthesis from nicotinamide (NAM) and nicotinamide riboside (NR), while down-regulating other NAD biosynthetic pathways. We show that overexpression of PARP10 is sufficient to depress cellular NAD and that the activities of the transcriptionally induced enzymes PARP7, PARP10, PARP12 and PARP14 are limited by cellular NAD and can be enhanced by pharmacological activation of NAD synthesis. We further demonstrate that infection with MHV induces a severe attack on host cell NAD
MeSH term(s)	A549 Cells ; ADP-Ribosylation ; Adenosine Diphosphate Ribose/metabolism ; Adult ; Animals ; COVID-19/immunology ; COVID-19/metabolism ; Cell Line, Tumor ; Female ; Ferrets ; Humans ; Immunity, Innate ; Male ; Metabolome ; Mice ; Mice, Inbred C57BL ; NAD/immunology ; NAD/metabolism ; Niacinamide/analogs & derivatives ; Niacinamide/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerases/blood ; Poly(ADP-ribose) Polymerases/immunology ; Pyridinium Compounds ; SARS-CoV-2/immunology ; SARS-CoV-2/metabolism
Chemical Substances	Poly(ADP-ribose) Polymerase Inhibitors ; Pyridinium Compounds ; nicotinamide-beta-riboside (0I8H2M0L7N) ; NAD (0U46U6E8UK) ; Adenosine Diphosphate Ribose (20762-30-5) ; Niacinamide (25X51I8RD4) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
Keywords	covid19
Language	English
Publishing date	2020-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA120.015138
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Uc I Zs.108: Show issues

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Article ; Online: Coronavirus Infection and PARP Expression Dysregulate the NAD Metabolome: A Potentially Actionable Component of Innate Immunity

Collin D. Heer / Daniel J. Sanderson / Yousef M.O. Alhammad / Mark S. Schmidt / Samuel A.J. Trammell / Stanley Perlman / Michael S. Cohen / Anthony R. Fehr / Charles Brenner

Abstract: AbstractOver the past several decades, multiple coronaviruses (CoVs) have emerged as highly infectious, lethal viruses in humans, most notably in the pandemic outbreak of COVID-19, the disease caused by SARS-CoV-2. To date, there are no known therapeutic ...

Abstract	AbstractOver the past several decades, multiple coronaviruses (CoVs) have emerged as highly infectious, lethal viruses in humans, most notably in the pandemic outbreak of COVID-19, the disease caused by SARS-CoV-2. To date, there are no known therapeutic or preventative agents to target CoVs. Though age and comorbidities severely increase case fatality rates, the host factors that influence resistance or susceptibility to infection with highly pathogenic human CoVs are unknown. Innate immune responses to CoVs are initiated by recognition of double-stranded (ds) RNA and induction of interferon, which turns on a gene expression program that inhibits viral replication. SARS-CoV-2 conserves an ADP-ribosylhydrolase domain previously shown to counteract innate immunity to both mouse hepatitis virus (MHV), a model CoV, and SARS-CoV. Here we show that SARS-CoV-2 infection of cell lines, infected ferrets, and a deceased patient’s lung consistently and strikingly dysregulates the nicotinamide adenine dinucleotide (NAD+) gene set with respect to NAD+ synthesis and utilization. SARS-CoV-2 induces a set of poly(ADP-ribose) polymerase (PARP) family members; these PARPs include enzymes required for the innate immune response to MHV. Further, we show that MHV infection induces an attack on host cell nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotide phosphate (NADP+). The data indicate that overexpression of a virally induced PARP, PARP10, is sufficient to depress host cell NAD metabolism and that NAD+ boosting strategies differ in their efficacy to restore PARP10 function. Gene expression and pharmacological data suggest that boosting NAD+ through the nicotinamide and nicotinamide riboside kinase pathways may restore antiviral PARP functions to support innate immunity to SARS-CoV-2, whereas PARP1,2 inhibition may be less likely to restore antiviral PARP functions.
Keywords	covid19
Publisher	biorxiv
Document type	Article ; Online
DOI	10.1101/2020.04.17.047480
Database	COVID19

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