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Article: Empagliflozin Decreases Lactate Generation in an NHE-1 Dependent Fashion and Increases α-Ketoglutarate Synthesis From Palmitate in Type II Diabetic Mouse Hearts.

Zhang, Hong / Uthman, Laween / Bakker, Diane / Sari, Sahinda / Chen, Sha / Hollmann, Markus W / Coronel, Ruben / Weber, Nina C / Houten, Sander M / van Weeghel, Michel / Zuurbier, Coert J

Frontiers in cardiovascular medicine

2020 Volume 7, Page(s) 592233

Abstract: Aims/hypothesis: ...

Abstract	Aims/hypothesis:
Language	English
Publishing date	2020-12-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2020.592233
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Article: Dietary restriction in the long-chain acyl-CoA dehydrogenase knockout mouse.

Diekman, Eugène F / van Weeghel, Michel / Suárez-Fariñas, Mayte / Argmann, Carmen / Ranea-Robles, Pablo / Wanders, Ronald J A / Visser, Gepke / van der Made, Ingeborg / Creemers, Esther E / Houten, Sander M

Molecular genetics and metabolism reports

2021 Volume 27, Page(s) 100749

Abstract: Patients with a disorder of mitochondrial long-chain fatty acid β-oxidation (FAO) have reduced fasting tolerance and may present with hypoketotic hypoglycemia, hepatomegaly, (cardio)myopathy and rhabdomyolysis. Patients should avoid a catabolic state ... ...

Abstract	Patients with a disorder of mitochondrial long-chain fatty acid β-oxidation (FAO) have reduced fasting tolerance and may present with hypoketotic hypoglycemia, hepatomegaly, (cardio)myopathy and rhabdomyolysis. Patients should avoid a catabolic state because it increases reliance on FAO as energy source. It is currently unclear whether weight loss through a reduction of caloric intake is safe in patients with a FAO disorder. We used the long-chain acyl-CoA dehydrogenase knockout (LCAD KO) mouse model to study the impact of dietary restriction (DR) on the plasma metabolite profile and cardiac function. For this, LCAD KO and wild type (WT) mice were subjected to DR (70% of ad libitum chow intake) for 4 weeks and compared to ad libitum chow fed mice. We found that DR had a relatively small impact on the plasma metabolite profile of WT and LCAD KO mice. Echocardiography revealed a small decrease in left ventricular systolic function of LCAD KO mice, which was most noticeable after DR, but there was no evidence of DR-induced cardiac remodeling. Our results suggest that weight loss through DR does not have acute and detrimental consequences in a mouse model for FAO disorders.
Language	English
Publishing date	2021-03-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821908-9
ISSN	2214-4269
ISSN	2214-4269
DOI	10.1016/j.ymgmr.2021.100749
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Article ; Online: Dietary restriction in the long-chain acyl-CoA dehydrogenase knockout mouse

Eugène F. Diekman / Michel van Weeghel / Mayte Suárez-Fariñas / Carmen Argmann / Pablo Ranea-Robles / Ronald J.A. Wanders / Gepke Visser / Ingeborg van der Made / Esther E. Creemers / Sander M. Houten

Molecular Genetics and Metabolism Reports, Vol 27, Iss , Pp 100749- (2021)

2021

Abstract	Patients with a disorder of mitochondrial long-chain fatty acid β-oxidation (FAO) have reduced fasting tolerance and may present with hypoketotic hypoglycemia, hepatomegaly, (cardio)myopathy and rhabdomyolysis. Patients should avoid a catabolic state because it increases reliance on FAO as energy source. It is currently unclear whether weight loss through a reduction of caloric intake is safe in patients with a FAO disorder. We used the long-chain acyl-CoA dehydrogenase knockout (LCAD KO) mouse model to study the impact of dietary restriction (DR) on the plasma metabolite profile and cardiac function. For this, LCAD KO and wild type (WT) mice were subjected to DR (70% of ad libitum chow intake) for 4 weeks and compared to ad libitum chow fed mice. We found that DR had a relatively small impact on the plasma metabolite profile of WT and LCAD KO mice. Echocardiography revealed a small decrease in left ventricular systolic function of LCAD KO mice, which was most noticeable after DR, but there was no evidence of DR-induced cardiac remodeling. Our results suggest that weight loss through DR does not have acute and detrimental consequences in a mouse model for FAO disorders.
Keywords	Mouse model ; Dietary restriction ; Caloric restriction ; Fatty acid oxidation ; Cardiac function ; Inborn error of metabolism ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: NLRX1 Deletion Increases Ischemia-Reperfusion Damage and Activates Glucose Metabolism in Mouse Heart.

Zhang, Hong / Xiao, Yang / Nederlof, Rianne / Bakker, Diane / Zhang, Pengbo / Girardin, Stephen E / Hollmann, Markus W / Weber, Nina C / Houten, Sander M / van Weeghel, Michel / Kibbey, Richard G / Zuurbier, Coert J

Frontiers in immunology

2020 Volume 11, Page(s) 591815

Abstract: Background: NOD-like receptors (NLR) are intracellular sensors of the innate immune system, with the NLRP3 being a pro-inflammatory member that modulates cardiac ischemia-reperfusion injury (IRI) and metabolism. No information is available on a possible ...

Abstract	Background: NOD-like receptors (NLR) are intracellular sensors of the innate immune system, with the NLRP3 being a pro-inflammatory member that modulates cardiac ischemia-reperfusion injury (IRI) and metabolism. No information is available on a possible role of anti-inflammatory NLRs on IRI and metabolism in the intact heart. Here we hypothesize that the constitutively expressed, anti-inflammatory mitochondrial NLRX1, affects IRI and metabolism of the isolated mouse heart. Methods: Isolated C57Bl/6J and NLRX1 knock-out (KO) mouse hearts were perfused with a physiological mixture of the essential substrates (lactate, glucose, pyruvate, fatty acid, glutamine) and insulin. For the IRI studies, hearts were subjected to either mild (20 min) or severe (35 min) ischemia and IRI was determined at 60 min reperfusion. Inflammatory mediators (IL-6, TNFα) and survival pathways (mito-HKII, p-Akt, p-AMPK, p-STAT3) were analyzed at 5 min of reperfusion. For the metabolism studies, hearts were perfused for 35 min with either 5.5 mM Results: NLRX1 KO significantly increased IRI (infarct size from 63% to 73%, end-diastolic pressure from 59 mmHg to 75 mmHg, and rate-pressure-product recovery from 15% to 6%), following severe, but not mild, ischemia. The increased IRI in NLRX1 KO hearts was associated with depressed Akt signaling at early reperfusion; other survival pathways or inflammatory parameters were not affected. Metabolically, NLRX1 KO hearts displayed increased lactate production and glucose oxidation relative to fatty acid oxidation, associated with increased pyruvate dehydrogenase flux and 10% higher cardiac oxygen consumption. Conclusion: Deletion of the mitochondrially-located NOD-like sensor NLRX1 exacerbates severe cardiac IR injury, possibly through impaired Akt signaling, and increases cardiac glucose metabolism.
MeSH term(s)	Animals ; Biomarkers ; Carbohydrate Metabolism ; Cytokines/metabolism ; Disease Models, Animal ; Gene Deletion ; Glucose/metabolism ; Mice ; Mice, Knockout ; Mitochondrial Proteins/genetics ; Myocardial Reperfusion Injury/etiology ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Oxidation-Reduction ; Oxidative Stress ; Proto-Oncogene Proteins c-akt/metabolism
Chemical Substances	Biomarkers ; Cytokines ; Mitochondrial Proteins ; NLRX1 protein, mouse ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-12-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.591815
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Article ; Online: A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation.

Houten, Sander Michel / Wanders, Ronald J A

Journal of inherited metabolic disease

2010 Volume 33, Issue 5, Page(s) 469–477

Abstract: Over the years, the mitochondrial fatty acid β-oxidation (FAO) pathway has been characterised at the biochemical level as well as the molecular biological level. FAO plays a pivotal role in energy homoeostasis, but it competes with glucose as the primary ...

Abstract	Over the years, the mitochondrial fatty acid β-oxidation (FAO) pathway has been characterised at the biochemical level as well as the molecular biological level. FAO plays a pivotal role in energy homoeostasis, but it competes with glucose as the primary oxidative substrate. The mechanisms behind this so-called glucose-fatty acid cycle operate at the hormonal, transcriptional and biochemical levels. Inherited defects for most of the FAO enzymes have been identified and characterised and are currently included in neonatal screening programmes. Symptoms range from hypoketotic hypoglycaemia to skeletal and cardiac myopathies. The pathophysiology of these diseases is still not completely understood, hampering optimal treatment. Studies of patients and mouse models will contribute to our understanding of the pathogenesis and will ultimately lead to better treatment.
MeSH term(s)	Animals ; Disease Models, Animal ; Energy Metabolism/genetics ; Fatty Acids/metabolism ; Genotype ; Homeostasis ; Humans ; Lipid Metabolism, Inborn Errors/enzymology ; Lipid Metabolism, Inborn Errors/genetics ; Lipid Metabolism, Inborn Errors/physiopathology ; Mice ; Mitochondria/enzymology ; Mitochondrial Diseases/enzymology ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/physiopathology ; Oxidation-Reduction ; Phenotype
Chemical Substances	Fatty Acids
Language	English
Publishing date	2010-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	438341-2
ISSN	1573-2665 ; 0141-8955
ISSN (online)	1573-2665
ISSN	0141-8955
DOI	10.1007/s10545-010-9061-2
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Article: A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation

Houten, Sander Michel / Wanders, Ronald J. A

Journal of inherited metabolic disease. 2010 Oct., v. 33, no. 5

2010

Abstract	Over the years, the mitochondrial fatty acid β-oxidation (FAO) pathway has been characterised at the biochemical level as well as the molecular biological level. FAO plays a pivotal role in energy homoeostasis, but it competes with glucose as the primary oxidative substrate. The mechanisms behind this so-called glucose-fatty acid cycle operate at the hormonal, transcriptional and biochemical levels. Inherited defects for most of the FAO enzymes have been identified and characterised and are currently included in neonatal screening programmes. Symptoms range from hypoketotic hypoglycaemia to skeletal and cardiac myopathies. The pathophysiology of these diseases is still not completely understood, hampering optimal treatment. Studies of patients and mouse models will contribute to our understanding of the pathogenesis and will ultimately lead to better treatment.
Language	English
Dates of publication	2010-10
Size	p. 469-477.
Publisher	Springer Netherlands
Publishing place	Dordrecht
Document type	Article
ZDB-ID	438341-2
ISSN	1573-2665 ; 0141-8955
ISSN (online)	1573-2665
ISSN	0141-8955
DOI	10.1007/s10545-010-9061-2
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Article ; Online: Food withdrawal lowers energy expenditure and induces inactivity in long-chain fatty acid oxidation-deficient mouse models.

Diekman, Eugene F / van Weeghel, Michel / Wanders, Ronald J A / Visser, Gepke / Houten, Sander M

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2014 Volume 28, Issue 7, Page(s) 2891–2900

Abstract: ... Wanders, R. J. A., Visser, G., Houten, S. M. Food withdrawal lowers energy expenditure and induces ...

Abstract	Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is an inherited disorder of mitochondrial long-chain fatty acid β-oxidation (FAO). Patients with VLCAD deficiency may present with hypoglycemia, hepatomegaly, cardiomyopathy, and myopathy. Although several mouse models have been developed to aid in the study of the pathogenesis of long-chain FAO defects, the muscular phenotype is underexposed. To address the muscular phenotype, we used a newly developed mouse model on a mixed genetic background with a more severe defect in FAO (LCAD(-/-); VLCAD(+/-)) in addition to a validated mouse model (LCAD(-/-); VLCAD(+/+)) and compared them with wild-type (WT) mice. We found that both mouse models show a 20% reduction in energy expenditure (EE) and a 3-fold decrease in locomotor activity in the unfed state. In addition, we found a 1.7°C drop in body temperature in unfed LCAD(-/-); VLCAD(+/+) mice compared with WT body temperature. We conclude that food withdrawal-induced inactivity, hypothermia, and reduction in EE are novel phenotypes associated with FAO deficiency in mice. Unexpectedly, inactivity was not explained by rhabdomyolysis, but rather reflected the overall reduced capacity of these mice to generate heat. We suggest that mice are partly protected against the negative consequence of an FAO defect.-Diekman, E. F., van Weeghel, M., Wanders, R. J. A., Visser, G., Houten, S. M. Food withdrawal lowers energy expenditure and induces inactivity in long-chain fatty acid oxidation-deficient mouse models.
MeSH term(s)	Acyl-CoA Dehydrogenase, Long-Chain/deficiency ; Acyl-CoA Dehydrogenase, Long-Chain/metabolism ; Animals ; Body Temperature/physiology ; Cardiomegaly/metabolism ; Cardiomegaly/physiopathology ; Disease Models, Animal ; Energy Metabolism/physiology ; Fatty Acids/metabolism ; Fatty Liver/metabolism ; Fatty Liver/physiopathology ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Lipid Metabolism, Inborn Errors/metabolism ; Lipid Metabolism, Inborn Errors/physiopathology ; Mice ; Mice, Inbred C57BL ; Mitochondrial Diseases/metabolism ; Mitochondrial Diseases/physiopathology ; Motor Activity/physiology ; Muscular Diseases/metabolism ; Muscular Diseases/physiopathology ; Oxidation-Reduction ; Phenotype ; Rhabdomyolysis/metabolism ; Rhabdomyolysis/physiopathology
Chemical Substances	Fatty Acids ; Acyl-CoA Dehydrogenase, Long-Chain (EC 1.3.8.8)
Language	English
Publishing date	2014-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.14-250241
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Article ; Online: Carnitine supplementation attenuates myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice.

Bakermans, Adrianus J / van Weeghel, Michel / Denis, Simone / Nicolay, Klaas / Prompers, Jeanine J / Houten, Sander M

Journal of inherited metabolic disease

2013 Volume 36, Issue 6, Page(s) 973–981

Abstract: Purpose: Elevation of long-chain acylcarnitine levels is a hallmark of long-chain mitochondrial β-oxidation (FAO) disorders, and can be accompanied by secondary carnitine deficiency. To restore free carnitine levels, and to increase myocardial export of ...

Abstract	Purpose: Elevation of long-chain acylcarnitine levels is a hallmark of long-chain mitochondrial β-oxidation (FAO) disorders, and can be accompanied by secondary carnitine deficiency. To restore free carnitine levels, and to increase myocardial export of long-chain fatty acyl-CoA esters, supplementation of L-carnitine in patients has been proposed. However, carnitine supplementation is controversial, because it may enhance the potentially lipotoxic buildup of long-chain acylcarnitines in the FAO-deficient heart. In this longitudinal study, we investigated the effects of carnitine supplementation in an animal model of long-chain FAO deficiency, the long-chain acyl-CoA dehydrogenase (LCAD) knockout (KO) mouse. Methods: Cardiac size and function, and triglyceride (TG) levels were quantified using proton magnetic resonance imaging (MRI) and spectroscopy ((1)H-MRS) in LCAD KO and wild-type (WT) mice. Carnitine was supplemented orally for 4 weeks starting at 5 weeks of age. Non-supplemented animals served as controls. In vivo data were complemented with ex vivo biochemical assays. Results: LCAD KO mice displayed cardiac hypertrophy and elevated levels of myocardial TG compared to WT mice. Carnitine supplementation lowered myocardial TG, normalizing myocardial TG levels in LCAD KO mice. Furthermore, carnitine supplementation did not affect cardiac performance and hypertrophy, or induce an accumulation of potentially toxic long-chain acylcarnitines in the LCAD KO heart. Conclusion: This study lends support to the proposed beneficial effect of carnitine supplementation alleviating toxicity by exporting acylcarnitines out of the FAO-deficient myocardium, rather than to the concern about a potentially detrimental effect of supplementation-induced production of lipotoxic long-chain acylcarnitines.
MeSH term(s)	Acyl-CoA Dehydrogenase, Long-Chain/deficiency ; Acyl-CoA Dehydrogenase, Long-Chain/genetics ; Acyl-CoA Dehydrogenase, Long-Chain/metabolism ; Animals ; Carnitine/analogs & derivatives ; Carnitine/blood ; Carnitine/pharmacology ; Dietary Supplements ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Heart/drug effects ; Lipid Metabolism/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; Triglycerides/metabolism
Chemical Substances	Triglycerides ; acylcarnitine ; Acyl-CoA Dehydrogenase, Long-Chain (EC 1.3.8.8) ; Carnitine (S7UI8SM58A)
Language	English
Publishing date	2013-04-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	438341-2
ISSN	1573-2665 ; 0141-8955
ISSN (online)	1573-2665
ISSN	0141-8955
DOI	10.1007/s10545-013-9604-4
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Article ; Online: Increased cardiac fatty acid oxidation in a mouse model with decreased malonyl-CoA sensitivity of CPT1B.

van Weeghel, Michel / Abdurrachim, Desiree / Nederlof, Rianne / Argmann, Carmen A / Houtkooper, Riekelt H / Hagen, Jacob / Nabben, Miranda / Denis, Simone / Ciapaite, Jolita / Kolwicz, Stephen C / Lopaschuk, Gary D / Auwerx, Johan / Nicolay, Klaas / Des Rosiers, Christine / Wanders, Ronald J / Zuurbier, Coert J / Prompers, Jeanine J / Houten, Sander M

Cardiovascular research

2018 Volume 114, Issue 10, Page(s) 1324–1334

Abstract: Aims: Mitochondrial fatty acid oxidation (FAO) is an important energy provider for cardiac work and changes in cardiac substrate preference are associated with different heart diseases. Carnitine palmitoyltransferase 1B (CPT1B) is thought to perform the ...

Abstract	Aims: Mitochondrial fatty acid oxidation (FAO) is an important energy provider for cardiac work and changes in cardiac substrate preference are associated with different heart diseases. Carnitine palmitoyltransferase 1B (CPT1B) is thought to perform the rate limiting enzyme step in FAO and is inhibited by malonyl-CoA. The role of CPT1B in cardiac metabolism has been addressed by inhibiting or decreasing CPT1B protein or after modulation of tissue malonyl-CoA metabolism. We assessed the role of CPT1B malonyl-CoA sensitivity in cardiac metabolism. Methods and results: We generated and characterized a knock in mouse model expressing the CPT1BE3A mutant enzyme, which has reduced sensitivity to malonyl-CoA. In isolated perfused hearts, FAO was 1.9-fold higher in Cpt1bE3A/E3A hearts compared with Cpt1bWT/WT hearts. Metabolomic, proteomic and transcriptomic analysis showed increased levels of malonylcarnitine, decreased concentration of CPT1B protein and a small but coordinated downregulation of the mRNA expression of genes involved in FAO in Cpt1bE3A/E3A hearts, all of which aim to limit FAO. In vivo assessment of cardiac function revealed only minor changes, cardiac hypertrophy was absent and histological analysis did not reveal fibrosis. Conclusions: Malonyl-CoA-dependent inhibition of CPT1B plays a crucial role in regulating FAO rate in the heart. Chronic elevation of FAO has a relatively subtle impact on cardiac function at least under baseline conditions.
MeSH term(s)	Animals ; Carnitine O-Palmitoyltransferase/genetics ; Carnitine O-Palmitoyltransferase/metabolism ; Energy Metabolism ; Fatty Acids/metabolism ; Genotype ; Glucose/metabolism ; Glycolysis ; Isolated Heart Preparation ; Malonyl Coenzyme A/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondria, Heart/enzymology ; Mutation ; Myocardium/enzymology ; Oxidation-Reduction ; Phenotype ; Ventricular Function, Left
Chemical Substances	Fatty Acids ; Malonyl Coenzyme A (524-14-1) ; CPT1B protein, mouse (EC 2.3.1.21) ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvy089
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Article ; Online: Identification and characterization of Eci3, a murine kidney-specific Δ3,Δ2-enoyl-CoA isomerase.

van Weeghel, Michel / Ofman, Rob / Argmann, Carmen A / Ruiter, Jos P N / Claessen, Nike / Oussoren, Saskia V / Wanders, Ronald J A / Aten, Jan / Houten, Sander M

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2014 Volume 28, Issue 3, Page(s) 1365–1374

Abstract: Oxidation of unsaturated fatty acids requires the action of auxiliary enzymes, such as Δ(3),Δ(2)-enoyl-CoA isomerases. Here we describe a detailed biochemical, molecular, histological, and evolutionary characterization of Eci3, the fourth member of the ... ...

Abstract	Oxidation of unsaturated fatty acids requires the action of auxiliary enzymes, such as Δ(3),Δ(2)-enoyl-CoA isomerases. Here we describe a detailed biochemical, molecular, histological, and evolutionary characterization of Eci3, the fourth member of the mammalian enoyl-CoA isomerase family. Eci3 specifically evolved in rodents after gene duplication of Eci2. Eci3 is with 79% identity homologous to Eci2 and contains a peroxisomal targeting signal type 1. Subcellular fractionation of mouse kidney and immunofluorescence studies revealed a specific peroxisomal localization for Eci3. Expression studies showed that mouse Eci3 is almost exclusively expressed in kidney. By using immunohistochemistry, we found that Eci3 is not only expressed in cells of the proximal tubule, but also in a subset of cells in the tubulointerstitium and the glomerulus. In vitro, Eci3 catalyzed the isomerization of trans-3-nonenoyl-CoA to trans-2-nonenoyl-CoA equally efficient as Eci2, suggesting a role in oxidation of unsaturated fatty acids. However, in contrast to Eci2, in silico gene coexpression and enrichment analysis for Eci3 in kidney did not yield carboxylic acid metabolism, but diverse biological functions, such as ion transport (P=7.1E-3) and tissue morphogenesis (P=1.0E-3). Thus, Eci3 picked up a novel and unexpected role in kidney function during rodent evolution.
MeSH term(s)	Animals ; Base Sequence ; DNA Primers ; Dodecenoyl-CoA Isomerase/metabolism ; Fluorescent Antibody Technique ; Humans ; Kidney/enzymology ; Mice
Chemical Substances	DNA Primers ; Dodecenoyl-CoA Isomerase (EC 5.3.3.8)
Language	English
Publishing date	2014-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.13-240416
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