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Article ; Online: Multidrug resistance proteins preferentially regulate natriuretic peptide-driven cGMP signalling in the heart and vasculature.

Grange, Robert M H / Preedy, Michael E J / Renukanthan, Aniruthan / Dignam, Joshua P / Lowe, Vanessa J / Moyes, Amie J / Pérez-Ternero, Cristina / Aubdool, Aisah A / Baliga, Reshma S / Hobbs, Adrian J

British journal of pharmacology

2021 Volume 179, Issue 11, Page(s) 2443–2459

Abstract: Background and purpose: cGMP underpins the bioactivity of NO and natriuretic peptides and is key to cardiovascular homeostasis. cGMP-driven responses are terminated primarily by PDEs, but cellular efflux via multidrug resistance proteins (MRPs) might ... ...

Abstract	Background and purpose: cGMP underpins the bioactivity of NO and natriuretic peptides and is key to cardiovascular homeostasis. cGMP-driven responses are terminated primarily by PDEs, but cellular efflux via multidrug resistance proteins (MRPs) might contribute. Herein, the effect of pharmacological blockade of MRPs on cGMP signalling in the heart and vasculature was investigated in vitro and in vivo. Experimental approach: Proliferation of human coronary artery smooth muscle cells (hCASMCs), vasorelaxation of murine aorta and reductions in mean arterial BP (MABP) in response to NO donors or natriuretic peptides were determined in the absence and presence of the MRP inhibitor MK571. The ability of MRP inhibition to reverse morphological and contractile deficits in a murine model of pressure overload-induced heart failure was also explored. Key results: MK571 attenuated hCASMC growth and enhanced the anti-proliferative effects of NO and atrial natriuretic peptide (ANP). MRP blockade caused concentration-dependent relaxations of murine aorta and augmented responses to ANP (and to a lesser extent NO). MK571 did not decrease MABP per se but enhanced the hypotensive actions of ANP and improved structural and functional indices of disease severity in experimental heart failure. These beneficial actions of MRP inhibition were associated with a greater intracellular:extracellular cGMP ratio in vitro and in vivo. Conclusions and implications: MRP blockade promotes the cardiovascular functions of natriuretic peptides in vitro and in vivo, with more modest effects on NO. MRP inhibition may have therapeutic utility in cardiovascular diseases triggered by dysfunctional cGMP signalling, particularly those associated with altered natriuretic peptide bioactivity. Linked articles: This article is part of a themed issue on cGMP Signalling in Cell Growth and Survival. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.11/issuetoc.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B ; Animals ; Atrial Natriuretic Factor/metabolism ; Atrial Natriuretic Factor/pharmacology ; Cyclic GMP/metabolism ; Heart Failure/drug therapy ; Humans ; Mice ; Natriuretic Peptides/metabolism ; Vasodilator Agents
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B ; Natriuretic Peptides ; Vasodilator Agents ; Atrial Natriuretic Factor (85637-73-6) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2021-07-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15593
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Article ; Online: Electronic cigarette vaping with aged coils causes acute lung injury in mice.

Goto, Shunsaku / Grange, Robert M H / Pinciroli, Riccardo / Rosales, Ivy A / Li, Rebecca / Boerboom, Sophie L / Ostrom, Katrina F / Marutani, Eizo / Wanderley, Hatus V / Bagchi, Aranya / Colvin, Robert B / Berra, Lorenzo / Minaeva, Olga / Goldstein, Lee E / Malhotra, Rajeev / Zapol, Warren M / Ichinose, Fumito / Yu, Binglan

Archives of toxicology

2022 Volume 96, Issue 12, Page(s) 3363–3371

Abstract: Electronic cigarettes (e-cigarettes) have been used widely as an alternative to conventional cigarettes and have become particularly popular among young adults. A growing body of evidence has shown that e-cigarettes are associated with acute lung injury ... ...

Abstract	Electronic cigarettes (e-cigarettes) have been used widely as an alternative to conventional cigarettes and have become particularly popular among young adults. A growing body of evidence has shown that e-cigarettes are associated with acute lung injury and adverse effects in multiple other organs. Previous studies showed that high emissions of aldehydes (formaldehyde and acetaldehyde) in aerosols were associated with increased usage of the same e-cigarette coils. However, the impact on lung function of using aged coils has not been reported. We investigated the relationship between coil age and acute lung injury in mice exposed to experimental vaping for 1 h (2 puffs/min, 100 ml/puff). The e-liquid contains propylene glycol and vegetable glycerin (50:50, vol) only. The concentrations of formaldehyde and acetaldehyde in the vaping aerosols increased with age of the nichrome coils starting at 1200 puffs. Mice exposed to e-cigarette aerosols produced from 1800, but not 0 or 900, puff-aged coils caused acute lung injury, increased lung wet/dry weight ratio, and induced lung inflammation (IL-6, TNF-α, IL-1β, MIP-2). Exposure to vaping aerosols from 1800 puff-aged coils decreased heart rate, respiratory rate, and oxygen saturation in mice compared to mice exposed to air or aerosols from new coils. In conclusion, we observed that the concentration of aldehydes (formaldehyde and acetaldehyde) increased with repeated and prolonged usage of e-cigarette coils. Exposure to high levels of aldehyde in vaping aerosol was associated with acute lung injury in mice. These findings show significant risk of lung injury associated with prolonged use of e-cigarette devices.
MeSH term(s)	Animals ; Mice ; Acetaldehyde ; Acute Lung Injury/chemically induced ; Aldehydes/toxicity ; Electronic Nicotine Delivery Systems ; Formaldehyde/toxicity ; Glycerol ; Interleukin-6 ; Propylene Glycol/toxicity ; Respiratory Aerosols and Droplets ; Tumor Necrosis Factor-alpha ; Vaping
Chemical Substances	Acetaldehyde (GO1N1ZPR3B) ; Aldehydes ; Formaldehyde (1HG84L3525) ; Glycerol (PDC6A3C0OX) ; Interleukin-6 ; Propylene Glycol (6DC9Q167V3) ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2022-10-04
Publishing country	Germany
Document type	Journal Article
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-022-03388-x
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Article ; Online: Airway stem cells sense hypoxia and differentiate into protective solitary neuroendocrine cells.

Shivaraju, Manjunatha / Chitta, Udbhav K / Grange, Robert M H / Jain, Isha H / Capen, Diane / Liao, Lan / Xu, Jianming / Ichinose, Fumito / Zapol, Warren M / Mootha, Vamsi K / Rajagopal, Jayaraj

Science (New York, N.Y.)

2021 Volume 371, Issue 6524, Page(s) 52–57

Abstract: Neuroendocrine (NE) cells are epithelial cells that possess many of the characteristics of neurons, including the presence of secretory vesicles and the ability to sense environmental stimuli. The normal physiologic functions of solitary airway NE cells ... ...

Abstract	Neuroendocrine (NE) cells are epithelial cells that possess many of the characteristics of neurons, including the presence of secretory vesicles and the ability to sense environmental stimuli. The normal physiologic functions of solitary airway NE cells remain a mystery. We show that mouse and human airway basal stem cells sense hypoxia. Hypoxia triggers the direct differentiation of these stem cells into solitary NE cells. Ablation of these solitary NE cells during hypoxia results in increased epithelial injury, whereas the administration of the NE cell peptide CGRP rescues this excess damage. Thus, we identify stem cells that directly sense hypoxia and respond by differentiating into solitary NE cells that secrete a protective peptide that mitigates hypoxic injury.
MeSH term(s)	Anaerobiosis ; Animals ; Calcitonin Gene-Related Peptide/metabolism ; Calcitonin Gene-Related Peptide/pharmacology ; Calcitonin Receptor-Like Protein/metabolism ; Cell Count ; Cell Differentiation ; Gene Deletion ; Humans ; Hypoxia/metabolism ; Hypoxia/pathology ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Mice ; Mice, Mutant Strains ; Neuroendocrine Cells/cytology ; Neuroendocrine Cells/physiology ; Oxygen/physiology ; Prolyl Hydroxylases/metabolism ; Stem Cells/cytology ; Stem Cells/drug effects ; Stem Cells/physiology ; Trachea/cytology ; Trans-Activators/genetics
Chemical Substances	Calcitonin Receptor-Like Protein ; Hypoxia-Inducible Factor 1, alpha Subunit ; Trans-Activators ; Trp63 protein, mouse ; Prolyl Hydroxylases (EC 1.14.11.-) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z) ; Oxygen (S88TT14065)
Language	English
Publishing date	2021-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aba0629
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Article ; Online: Electronic cigarette vaping with aged coils causes acute lung injury in mice

Goto, Shunsaku / Grange, Robert M. H. / Pinciroli, Riccardo / Rosales, Ivy A. / Li, Rebecca / Boerboom, Sophie L. / Ostrom, Katrina F. / Marutani, Eizo / Wanderley, Hatus V. / Bagchi, Aranya / Colvin, Robert B. / Berra, Lorenzo / Minaeva, Olga / Goldstein, Lee E. / Malhotra, Rajeev / Zapol, Warren M. / Ichinose, Fumito / Yu, Binglan

Arch Toxicol. 2022 Dec., v. 96, no. 12, p. 3363-3371

2022 , Page(s) 3363–3371

Abstract	Electronic cigarettes (e-cigarettes) have been used widely as an alternative to conventional cigarettes and have become particularly popular among young adults. A growing body of evidence has shown that e-cigarettes are associated with acute lung injury and adverse effects in multiple other organs. Previous studies showed that high emissions of aldehydes (formaldehyde and acetaldehyde) in aerosols were associated with increased usage of the same e-cigarette coils. However, the impact on lung function of using aged coils has not been reported. We investigated the relationship between coil age and acute lung injury in mice exposed to experimental vaping for 1 h (2 puffs/min, 100 ml/puff). The e-liquid contains propylene glycol and vegetable glycerin (50:50, vol) only. The concentrations of formaldehyde and acetaldehyde in the vaping aerosols increased with age of the nichrome coils starting at 1200 puffs. Mice exposed to e-cigarette aerosols produced from 1800, but not 0 or 900, puff-aged coils caused acute lung injury, increased lung wet/dry weight ratio, and induced lung inflammation (IL-6, TNF-α, IL-1β, MIP-2). Exposure to vaping aerosols from 1800 puff-aged coils decreased heart rate, respiratory rate, and oxygen saturation in mice compared to mice exposed to air or aerosols from new coils. In conclusion, we observed that the concentration of aldehydes (formaldehyde and acetaldehyde) increased with repeated and prolonged usage of e-cigarette coils. Exposure to high levels of aldehyde in vaping aerosol was associated with acute lung injury in mice. These findings show significant risk of lung injury associated with prolonged use of e-cigarette devices.
Keywords	acetaldehyde ; aerosols ; electronic equipment ; formaldehyde ; glycerol ; heart rate ; inflammation ; interleukin-6 ; lung function ; lungs ; oxygen ; propylene glycol ; respiratory rate ; risk ; vegetables
Language	English
Dates of publication	2022-12
Size	p. 3363-3371
Publishing place	Springer Berlin Heidelberg
Document type	Article ; Online
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-022-03388-x
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Article ; Online: Identification of Candidate miRNA Biomarkers for Glaucoma.

Hindle, Allyson G / Thoonen, Robrecht / Jasien, Jessica V / Grange, Robert M H / Amin, Krishna / Wise, Jasen / Ozaki, Mineo / Ritch, Robert / Malhotra, Rajeev / Buys, Emmanuel S

Investigative ophthalmology & visual science

2019 Volume 60, Issue 1, Page(s) 134–146

Abstract: Purpose: Glaucoma, a leading cause of blindness worldwide, often remains undetected until irreversible vision loss has occurred. Treatments focus on lowering intraocular pressure (IOP), the only modifiable and readily measurable risk factor. However, ... ...

Abstract	Purpose: Glaucoma, a leading cause of blindness worldwide, often remains undetected until irreversible vision loss has occurred. Treatments focus on lowering intraocular pressure (IOP), the only modifiable and readily measurable risk factor. However, IOP can vary and does not always predict disease progression. MicroRNAs (miRNAs) are promising biomarkers. They are abundant and stable in biological fluids, including plasma and aqueous humor (AqH). We aimed to identify differentially expressed miRNAs in AqH and plasma from glaucoma, exfoliation syndrome (XFS), and control subjects. Methods: Plasma and AqH from two ethnic cohorts were harvested from glaucoma or XFS (often associated with glaucoma, n = 33) and control (n = 31) patients undergoing elective surgery. A custom miRNA array measured 372 miRNAs. Molecular target prediction and pathway analysis were performed with Ingenuity Pathway Analysis (IPA) and DIANA bioinformatical tools. Results: Levels of miRNAs in plasma, a readily accessible biomarker source, correlated with miRNA levels in AqH. Twenty circulating miRNAs were at least 1.5-fold higher in glaucoma or XFS patients than in controls across two ethnic cohorts: miR-4667-5p (P = 4.1 × 10-5), miR-99b-3p (P = 4.8 × 10-5), miR-637 (P = 5.1 × 10-5), miR-4490 (P = 5.7 × 10-5), miR-1253 (P = 6.0 × 10-5), miR-3190-3p (P = 3.1 × 10-4), miR-3173-3p (P = 0.001), miR-608 (P = 0.001), miR-4725-3p (P = 0.002), miR-4448 (P = 0.002), and miR-323b-5p (P = 0.002), miR-4538 (P = 0.003), miR-3913-3p (P = 0.003), miR-3159 (P = 0.003), miR-4663 (P = 0.003), miR-4767 (P = 0.003), miR-4724-5p (P = 0.003), miR-1306-5p (P = 0.003), miR-181b-3p (P = 0.004), and miR-433-3p (P = 0.004). miR-637, miR-1306-5p, and miR-3159, in combination, allowed discrimination between glaucoma patients and control subjects (AUC = 0.91 ± 0.008, sensitivity 85.0%, specificity 87.5%). Conclusions: These results identify specific miRNAs as potential biomarkers and provide insight into the molecular processes underlying glaucoma.
MeSH term(s)	Aged ; Aged, 80 and over ; Aqueous Humor/metabolism ; Asian Continental Ancestry Group/ethnology ; Biomarkers/blood ; European Continental Ancestry Group/ethnology ; Exfoliation Syndrome/blood ; Exfoliation Syndrome/ethnology ; Exfoliation Syndrome/surgery ; Female ; Gene Expression Profiling ; Glaucoma, Open-Angle/blood ; Glaucoma, Open-Angle/ethnology ; Glaucoma, Open-Angle/surgery ; Humans ; Intraocular Pressure ; Japan/epidemiology ; Male ; MicroRNAs/blood ; Middle Aged ; Polymerase Chain Reaction ; Sensitivity and Specificity ; United States/epidemiology
Chemical Substances	Biomarkers ; MicroRNAs
Language	English
Publishing date	2019-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.18-24878
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Article: Hypoxia Rescues Frataxin Loss by Restoring Iron Sulfur Cluster Biogenesis

Ast, Tslil / Meisel, Joshua D / Patra, Shachin / Wang, Hong / Grange, Robert M.H / Kim, Sharon H / Calvo, Sarah E / Orefice, Lauren L / Nagashima, Fumiaki / Ichinose, Fumito / Zapol, Warren M / Ruvkun, Gary / Barondeau, David P / Mootha, Vamsi K

Cell. 2019 May 30, v. 177, no. 6

2019

Abstract: Friedreich’s ataxia (FRDA) is a devastating, multisystemic disorder caused by recessive mutations in the mitochondrial protein frataxin (FXN). FXN participates in the biosynthesis of Fe-S clusters and is considered to be essential for viability. Here we ... ...

Abstract	Friedreich’s ataxia (FRDA) is a devastating, multisystemic disorder caused by recessive mutations in the mitochondrial protein frataxin (FXN). FXN participates in the biosynthesis of Fe-S clusters and is considered to be essential for viability. Here we report that when grown in 1% ambient O2, FXN null yeast, human cells, and nematodes are fully viable. In human cells, hypoxia restores steady-state levels of Fe-S clusters and normalizes ATF4, NRF2, and IRP2 signaling events associated with FRDA. Cellular studies and in vitro reconstitution indicate that hypoxia acts through HIF-independent mechanisms that increase bioavailable iron as well as directly activate Fe-S synthesis. In a mouse model of FRDA, breathing 11% O2 attenuates the progression of ataxia, whereas breathing 55% O2 hastens it. Our work identifies oxygen as a key environmental variable in the pathogenesis associated with FXN depletion, with important mechanistic and therapeutic implications.
Keywords	Nematoda ; animal models ; ataxia (disorder) ; bioavailability ; biogenesis ; biosynthesis ; breathing ; humans ; hypoxia ; iron ; mitochondria ; mutation ; oxygen ; pathogenesis ; sulfur ; therapeutics ; viability ; yeasts
Language	English
Dates of publication	2019-0530
Size	p. 1507-1521.e16.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2019.03.045
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Article ; Online: Hypoxia ameliorates brain hyperoxia and NAD

Grange, Robert M H / Sharma, Rohit / Shah, Hardik / Reinstadler, Bryn / Goldberger, Olga / Cooper, Marissa K / Nakagawa, Akito / Miyazaki, Yusuke / Hindle, Allyson G / Batten, Annabelle J / Wojtkiewicz, Gregory R / Schleifer, Grigorij / Bagchi, Aranya / Marutani, Eizo / Malhotra, Rajeev / Bloch, Donald B / Ichinose, Fumito / Mootha, Vamsi K / Zapol, Warren M

Molecular genetics and metabolism

2021 Volume 133, Issue 1, Page(s) 83–93

Abstract: Leigh syndrome is a severe mitochondrial neurodegenerative disease with no effective treatment. In the ... ...

Abstract	Leigh syndrome is a severe mitochondrial neurodegenerative disease with no effective treatment. In the Ndufs4
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Cell Hypoxia/physiology ; Disease Models, Animal ; Electron Transport Complex I/genetics ; Electron Transport Complex I/metabolism ; Humans ; Leigh Disease/genetics ; Leigh Disease/metabolism ; Leigh Disease/therapy ; Metabolomics ; Mice ; Mitochondria ; NAD/deficiency ; NAD/genetics ; Neurodegenerative Diseases ; Oxygen/metabolism ; Respiration/genetics
Chemical Substances	Ndufs4 protein, mouse ; NAD (0U46U6E8UK) ; Electron Transport Complex I (EC 7.1.1.2) ; Oxygen (S88TT14065)
Language	English
Publishing date	2021-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1418518-0
ISSN	1096-7206 ; 1096-7192
ISSN (online)	1096-7206
ISSN	1096-7192
DOI	10.1016/j.ymgme.2021.03.005
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Article ; Online: Hypoxia Rescues Frataxin Loss by Restoring Iron Sulfur Cluster Biogenesis.

Ast, Tslil / Meisel, Joshua D / Patra, Shachin / Wang, Hong / Grange, Robert M H / Kim, Sharon H / Calvo, Sarah E / Orefice, Lauren L / Nagashima, Fumiaki / Ichinose, Fumito / Zapol, Warren M / Ruvkun, Gary / Barondeau, David P / Mootha, Vamsi K

Cell

2019 Volume 177, Issue 6, Page(s) 1507–1521.e16

Abstract: Friedreich's ataxia (FRDA) is a devastating, multisystemic disorder caused by recessive mutations in the mitochondrial protein frataxin (FXN). FXN participates in the biosynthesis of Fe-S clusters and is considered to be essential for viability. Here we ... ...

Abstract	Friedreich's ataxia (FRDA) is a devastating, multisystemic disorder caused by recessive mutations in the mitochondrial protein frataxin (FXN). FXN participates in the biosynthesis of Fe-S clusters and is considered to be essential for viability. Here we report that when grown in 1% ambient O
MeSH term(s)	Activating Transcription Factor 4/metabolism ; Animals ; Caenorhabditis elegans/metabolism ; Female ; Friedreich Ataxia/metabolism ; HEK293 Cells ; Humans ; Hypoxia/metabolism ; Hypoxia/physiopathology ; Iron/metabolism ; Iron Regulatory Protein 2/metabolism ; Iron-Binding Proteins/metabolism ; Iron-Binding Proteins/physiology ; Iron-Sulfur Proteins/metabolism ; Iron-Sulfur Proteins/physiology ; K562 Cells ; Male ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Saccharomyces cerevisiae/metabolism ; Sulfur/metabolism ; Frataxin
Chemical Substances	ATF4 protein, human ; Iron-Binding Proteins ; Iron-Sulfur Proteins ; Mitochondrial Proteins ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Activating Transcription Factor 4 (145891-90-3) ; Sulfur (70FD1KFU70) ; Iron (E1UOL152H7) ; Iron Regulatory Protein 2 (EC 4.2.1.3)
Language	English
Publishing date	2019-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2019.03.045
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Article ; Online: Sulfide catabolism ameliorates hypoxic brain injury.

Marutani, Eizo / Morita, Masanobu / Hirai, Shuichi / Kai, Shinichi / Grange, Robert M H / Miyazaki, Yusuke / Nagashima, Fumiaki / Traeger, Lisa / Magliocca, Aurora / Ida, Tomoaki / Matsunaga, Tetsuro / Flicker, Daniel R / Corman, Benjamin / Mori, Naohiro / Yamazaki, Yumiko / Batten, Annabelle / Li, Rebecca / Tanaka, Tomohiro / Ikeda, Takamitsu /

Nakagawa, Akito / Atochin, Dmitriy N / Ihara, Hideshi / Olenchock, Benjamin A / Shen, Xinggui / Nishida, Motohiro / Hanaoka, Kenjiro / Kevil, Christopher G / Xian, Ming / Bloch, Donald B / Akaike, Takaaki / Hindle, Allyson G / Motohashi, Hozumi / Ichinose, Fumito

Nature communications

2021 Volume 12, Issue 1, Page(s) 3108

Abstract: The mammalian brain is highly vulnerable to oxygen deprivation, yet the mechanism underlying the brain's sensitivity to hypoxia is incompletely understood. Hypoxia induces accumulation of hydrogen sulfide, a gas that inhibits mitochondrial respiration. ... ...

Abstract	The mammalian brain is highly vulnerable to oxygen deprivation, yet the mechanism underlying the brain's sensitivity to hypoxia is incompletely understood. Hypoxia induces accumulation of hydrogen sulfide, a gas that inhibits mitochondrial respiration. Here, we show that, in mice, rats, and naturally hypoxia-tolerant ground squirrels, the sensitivity of the brain to hypoxia is inversely related to the levels of sulfide:quinone oxidoreductase (SQOR) and the capacity to catabolize sulfide. Silencing SQOR increased the sensitivity of the brain to hypoxia, whereas neuron-specific SQOR expression prevented hypoxia-induced sulfide accumulation, bioenergetic failure, and ischemic brain injury. Excluding SQOR from mitochondria increased sensitivity to hypoxia not only in the brain but also in heart and liver. Pharmacological scavenging of sulfide maintained mitochondrial respiration in hypoxic neurons and made mice resistant to hypoxia. These results illuminate the critical role of sulfide catabolism in energy homeostasis during hypoxia and identify a therapeutic target for ischemic brain injury.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Brain Injuries/genetics ; Brain Injuries/metabolism ; Cells, Cultured ; Female ; Hydrogen Sulfide/metabolism ; Hypoxia ; Male ; Membrane Potential, Mitochondrial ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Knockout ; Mitochondria/metabolism ; NAD/metabolism ; Quinone Reductases/genetics ; Quinone Reductases/metabolism ; RNA Interference ; Rats, Sprague-Dawley ; Mice ; Rats
Chemical Substances	NAD (0U46U6E8UK) ; Quinone Reductases (EC 1.6.99.-) ; sulfide quinone reductase (EC 1.8.5.-) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2021-05-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-23363-x
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In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito