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Article ; Online: Mitochondrial functional resilience after TFAM ablation in the adult heart.

Ghazal, Nasab / Peoples, Jessica N / Mohiuddin, Tahmina A / Kwong, Jennifer Q

American journal of physiology. Cell physiology

2021 Volume 320, Issue 6, Page(s) C929–C942

Abstract: The nuclear genome-encoded mitochondrial DNA (mtDNA) transcription factor A (TFAM) is indispensable for mitochondrial energy production in the developing and postnatal heart; a similar role for TFAM is inferred in adult heart. Here, we provide evidence ... ...

Abstract	The nuclear genome-encoded mitochondrial DNA (mtDNA) transcription factor A (TFAM) is indispensable for mitochondrial energy production in the developing and postnatal heart; a similar role for TFAM is inferred in adult heart. Here, we provide evidence that challenges this long-standing paradigm. Unexpectedly, conditional
MeSH term(s)	Animals ; DNA Replication/genetics ; DNA, Mitochondrial/genetics ; DNA-Binding Proteins/genetics ; Down-Regulation/genetics ; Electron Transport/genetics ; Female ; Gene Expression Regulation/genetics ; Heart/physiology ; High Mobility Group Proteins/genetics ; Male ; Mice ; Mitochondria/genetics ; Mitochondrial Proteins/genetics ; Myocytes, Cardiac/metabolism ; Transcription Factors/genetics ; Transcription, Genetic/genetics
Chemical Substances	DNA, Mitochondrial ; DNA-Binding Proteins ; High Mobility Group Proteins ; Mitochondrial Proteins ; Tfam protein, mouse ; Transcription Factors
Language	English
Publishing date	2021-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00508.2020
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Article: Mitochondrial citrate carrier SLC25A1 is a dosage-dependent regulator of metabolic reprogramming and morphogenesis in the developing heart.

Ohanele, Chiemela / Peoples, Jessica N / Karlstaedt, Anja / Geiger, Joshua T / Gayle, Ashley D / Ghazal, Nasab / Sohani, Fateemaa / Brown, Milton E / Davis, Michael E / Porter, George A / Faundez, Victor / Kwong, Jennifer Q

bioRxiv : the preprint server for biology

2023

Abstract: The developing mammalian heart undergoes an important metabolic shift from glycolysis toward mitochondrial oxidation, such that oxidative phosphorylation defects may present with cardiac abnormalities. Here, we describe a new mechanistic link between ... ...

Abstract	The developing mammalian heart undergoes an important metabolic shift from glycolysis toward mitochondrial oxidation, such that oxidative phosphorylation defects may present with cardiac abnormalities. Here, we describe a new mechanistic link between mitochondria and cardiac morphogenesis, uncovered by studying mice with systemic loss of the mitochondrial citrate carrier SLC25A1.
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.22.541833
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Article ; Online: Intact calcium signaling in adrenergic-deficient embryonic mouse hearts.

Peoples, Jessica N / Taylor, David G / Katchman, Alexander N / Ebert, Steven N

Biochemical and biophysical research communications

2018 Volume 495, Issue 4, Page(s) 2547–2552

Abstract: Mouse embryos that lack the ability to produce the adrenergic hormones, norepinephrine (NE) and epinephrine (EPI), due to disruption of the dopamine beta-hydroxylase ( ... ...

Abstract	Mouse embryos that lack the ability to produce the adrenergic hormones, norepinephrine (NE) and epinephrine (EPI), due to disruption of the dopamine beta-hydroxylase (Dbh
MeSH term(s)	Adrenergic Agents/metabolism ; Animals ; Calcium/metabolism ; Calcium Signaling/physiology ; Epinephrine/metabolism ; Heart/embryology ; Mice ; Mice, Knockout ; Myocardium/metabolism ; Norepinephrine/metabolism
Chemical Substances	Adrenergic Agents ; Calcium (SY7Q814VUP) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2018--22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2017.12.155
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Article ; Online: Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome.

Peoples, Jessica N / Ghazal, Nasab / Duong, Duc M / Hardin, Katherine R / Manning, Janet R / Seyfried, Nicholas T / Faundez, Victor / Kwong, Jennifer Q

American journal of physiology. Cell physiology

2021 Volume 321, Issue 3, Page(s) C519–C534

Abstract: Mitochondria are recognized as signaling organelles, because under stress, mitochondria can trigger various signaling pathways to coordinate the cell's response. The specific pathway(s) engaged by mitochondria in response to mitochondrial energy defects ... ...

Abstract	Mitochondria are recognized as signaling organelles, because under stress, mitochondria can trigger various signaling pathways to coordinate the cell's response. The specific pathway(s) engaged by mitochondria in response to mitochondrial energy defects in vivo and in high-energy tissues like the heart are not fully understood. Here, we investigated cardiac pathways activated in response to mitochondrial energy dysfunction by studying mice with cardiomyocyte-specific loss of the mitochondrial phosphate carrier (SLC25A3), an established model that develops cardiomyopathy as a result of defective mitochondrial ATP synthesis. Mitochondrial energy dysfunction induced a striking pattern of acylome remodeling, with significantly increased posttranslational acetylation and malonylation. Mass spectrometry-based proteomics further revealed that energy dysfunction-induced remodeling of the acetylome and malonylome preferentially impacts mitochondrial proteins. Acetylation and malonylation modified a highly interconnected interactome of mitochondrial proteins, and both modifications were present on the enzyme isocitrate dehydrogenase 2 (IDH2). Intriguingly, IDH2 activity was enhanced in SLC25A3-deleted mitochondria, and further study of IDH2 sites targeted by both acetylation and malonylation revealed that these modifications can have site-specific and distinct functional effects. Finally, we uncovered a novel cross talk between the two modifications, whereby mitochondrial energy dysfunction-induced acetylation of sirtuin 5 (SIRT5), inhibited its function. Because SIRT5 is a mitochondrial deacylase with demalonylase activity, this finding suggests that acetylation can modulate the malonylome. Together, our results position acylations as an arm of the mitochondrial response to energy dysfunction and suggest a mechanism by which focal disruption to the energy production machinery can have an expanded impact on global mitochondrial function.
MeSH term(s)	Acetylation ; Animals ; Biological Transport ; Cardiomyopathies/genetics ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cation Transport Proteins/deficiency ; Cation Transport Proteins/genetics ; Energy Metabolism ; Female ; Gene Regulatory Networks ; Isocitrate Dehydrogenase/genetics ; Isocitrate Dehydrogenase/metabolism ; Male ; Malonates/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Heart/genetics ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/pathology ; Mitochondrial Proteins/deficiency ; Mitochondrial Proteins/genetics ; Models, Molecular ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Phosphate Transport Proteins/deficiency ; Phosphate Transport Proteins/genetics ; Phosphates ; Protein Conformation ; Protein Interaction Mapping ; Protein Processing, Post-Translational ; Signal Transduction ; Sirtuins/genetics ; Sirtuins/metabolism ; Solute Carrier Proteins/deficiency ; Solute Carrier Proteins/genetics
Chemical Substances	Cation Transport Proteins ; Malonates ; Mitochondrial Proteins ; Phosphate Transport Proteins ; Phosphates ; SIRT5 protein, mouse ; Slc25a3 protein, mouse ; Solute Carrier Proteins ; malonic acid (9KX7ZMG0MK) ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; isocitrate dehydrogenase 2, mouse (EC 1.1.1.41) ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00156.2021
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Article ; Online: Mitochondrial dysfunction and oxidative stress in heart disease.

Peoples, Jessica N / Saraf, Anita / Ghazal, Nasab / Pham, Tyler T / Kwong, Jennifer Q

Experimental & molecular medicine

2019 Volume 51, Issue 12, Page(s) 1–13

Abstract: Beyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated ... ...

Abstract	Beyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated process driving oxidative stress and disease pathology, contemporary studies reveal that ROS also facilitate normal physiology. Mitochondria are especially abundant in cardiac tissue; hence, mitochondrial dysregulation and ROS production are thought to contribute significantly to cardiac pathology. Moreover, there is growing appreciation that medical therapies designed to mediate mitochondrial ROS production can be important strategies to ameliorate cardiac disease. In this review, we highlight evidence from animal models that illustrates the strong connections between mitochondrial ROS and cardiac disease, discuss advancements in the development of mitochondria-targeted antioxidant therapies, and identify challenges faced in bringing such therapies into the clinic.
MeSH term(s)	Animals ; Cardiomyopathies/metabolism ; Heart Diseases/metabolism ; Humans ; Mitochondria/metabolism ; Mitochondrial Diseases/metabolism ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2019-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1328915-9
ISSN	2092-6413 ; 1226-3613 ; 0378-8512
ISSN (online)	2092-6413
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/s12276-019-0355-7
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Article: Intact calcium signaling in adrenergic-deficient embryonic mouse hearts

Peoples, Jessica N / Taylor, David G / Katchman, Alexander N / Ebert, Steven N

Biochemical and biophysical research communications. 2018 Jan. 22, v. 495, no. 4

2018

Abstract: Mouse embryos that lack the ability to produce the adrenergic hormones, norepinephrine (NE) and epinephrine (EPI), due to disruption of the dopamine beta-hydroxylase (Dbh−/-) gene inevitably perish from heart failure during mid-gestation. Since ... ...

Abstract	Mouse embryos that lack the ability to produce the adrenergic hormones, norepinephrine (NE) and epinephrine (EPI), due to disruption of the dopamine beta-hydroxylase (Dbh−/-) gene inevitably perish from heart failure during mid-gestation. Since adrenergic stimulation is well-known to enhance calcium signaling in developing as well as adult myocardium, and impairments in calcium signaling are typically associated with heart failure, we hypothesized that adrenergic-deficient embryonic hearts would display deficiencies in cardiac calcium signaling relative to adrenergic-competent controls at a developmental stage immediately preceding the onset of heart failure, which first appears beginning or shortly after mouse embryonic day 10.5 (E10.5). To test this hypothesis, we used ratiometric fluorescent calcium imaging techniques to measure cytosolic calcium transients, [Ca2+]i in isolated E10.5 mouse hearts. Our results show that spontaneous [Ca2+]i oscillations were intact and robustly responded to a variety of stimuli including extracellular calcium (5 mM), caffeine (5 mM), and NE (100 nM) in a manner that was indistinguishable from controls. Further, we show similar patterns of distribution (via immunofluorescent histochemical staining) and activity (via patch-clamp recording techniques) for the major voltage-gated plasma membrane calcium channel responsible for the L-type calcium current, ICa,L, in adrenergic-deficient and control embryonic cardiac cells. These results demonstrate that despite the absence of vital adrenergic hormones that consistently leads to embryonic lethality in vivo, intracellular and extracellular calcium signaling remain essentially intact and functional in embryonic mouse hearts through E10.5. These findings suggest that adrenergic stimulation is not required for the development of intracellular calcium oscillations or extracellular calcium signaling through ICa,L and that aberrant calcium signaling does not likely contribute to the onset of heart failure in this model.
Keywords	adults ; caffeine ; calcium ; calcium channels ; dopamine beta-monooxygenase ; embryonic mortality ; epinephrine ; fluorescence ; genes ; heart failure ; mice ; models ; myocardium ; norepinephrine ; plasma membrane ; pregnancy ; research
Language	English
Dates of publication	2018-0122
Size	p. 2547-2552.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2017.12.155
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Article ; Online: Metabolomics reveals critical adrenergic regulatory checkpoints in glycolysis and pentose-phosphate pathways in embryonic heart.

Peoples, Jessica N R / Maxmillian, Timmi / Le, Quynh / Nadtochiy, Sergiy M / Brookes, Paul S / Porter, George A / Davidson, Victor L / Ebert, Steven N

The Journal of biological chemistry

2018 Volume 293, Issue 18, Page(s) 6925–6941

Abstract: Cardiac energy demands during early embryonic periods are sufficiently met through glycolysis, but as development proceeds, the oxidative phosphorylation in mitochondria becomes increasingly vital. Adrenergic hormones are known to stimulate metabolism in ...

Abstract	Cardiac energy demands during early embryonic periods are sufficiently met through glycolysis, but as development proceeds, the oxidative phosphorylation in mitochondria becomes increasingly vital. Adrenergic hormones are known to stimulate metabolism in adult mammals and are essential for embryonic development, but relatively little is known about their effects on metabolism in the embryonic heart. Here, we show that embryos lacking adrenergic stimulation have ∼10-fold less cardiac ATP compared with littermate controls. Despite this deficit in steady-state ATP, neither the rates of ATP formation nor degradation was affected in adrenergic hormone-deficient hearts, suggesting that ATP synthesis and hydrolysis mechanisms were fully operational. We thus hypothesized that adrenergic hormones stimulate metabolism of glucose to provide chemical substrates for oxidation in mitochondria. To test this hypothesis, we employed a metabolomics-based approach using LC/MS. Our results showed glucose 1-phosphate and glucose 6-phosphate concentrations were not significantly altered, but several downstream metabolites in both glycolytic and pentose-phosphate pathways were significantly lower compared with controls. Furthermore, we identified glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase as key enzymes in those respective metabolic pathways whose activity was significantly (
MeSH term(s)	Adenosine Triphosphate/biosynthesis ; Adenosine Triphosphate/metabolism ; Animals ; Epinephrine/metabolism ; Female ; Glucose/metabolism ; Glucose-6-Phosphate/metabolism ; Glucosephosphate Dehydrogenase/metabolism ; Glucosephosphates/metabolism ; Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+)/metabolism ; Glycolysis ; Heart/embryology ; Hydrolysis ; Ketone Oxidoreductases/metabolism ; Male ; Metabolomics ; Mice, Inbred C57BL ; Mitochondria, Heart/metabolism ; Myocardium/metabolism ; Norepinephrine/metabolism ; Pentose Phosphate Pathway ; Phosphorylation ; Pregnancy
Chemical Substances	Glucosephosphates ; Glucose-6-Phosphate (56-73-5) ; Adenosine Triphosphate (8L70Q75FXE) ; glucose-1-phosphate (CIX3U01VAU) ; Glucosephosphate Dehydrogenase (EC 1.1.1.49) ; Ketone Oxidoreductases (EC 1.2.-) ; pyruvate dehydrogenase (NADP+) (EC 1.2.1.51) ; Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+) (EC 1.2.1.9) ; Glucose (IY9XDZ35W2) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2018-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA118.002566
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Article ; Online: Impaired cardiac energy metabolism in embryos lacking adrenergic stimulation.

Baker, Candice N / Gidus, Sarah A / Price, George F / Peoples, Jessica N R / Ebert, Steven N

American journal of physiology. Endocrinology and metabolism

2014 Volume 308, Issue 5, Page(s) E402–13

Abstract: As development proceeds from the embryonic to fetal stages, cardiac energy demands increase substantially, and oxidative phosphorylation of ADP to ATP in mitochondria becomes vital. Relatively little, however, is known about the signaling mechanisms ... ...

Abstract	As development proceeds from the embryonic to fetal stages, cardiac energy demands increase substantially, and oxidative phosphorylation of ADP to ATP in mitochondria becomes vital. Relatively little, however, is known about the signaling mechanisms regulating the transition from anaerobic to aerobic metabolism that occurs during the embryonic period. The main objective of this study was to test the hypothesis that adrenergic hormones provide critical stimulation of energy metabolism during embryonic/fetal development. We examined ATP and ADP concentrations in mouse embryos lacking adrenergic hormones due to targeted disruption of the essential dopamine β-hydroxylase (Dbh) gene. Embryonic ATP concentrations decreased dramatically, whereas ADP concentrations rose such that the ATP/ADP ratio in the adrenergic-deficient group was nearly 50-fold less than that found in littermate controls by embryonic day 11.5. We also found that cardiac extracellular acidification and oxygen consumption rates were significantly decreased, and mitochondria were significantly larger and more branched in adrenergic-deficient hearts. Notably, however, the mitochondria were intact with well-formed cristae, and there was no significant difference observed in mitochondrial membrane potential. Maternal administration of the adrenergic receptor agonists isoproterenol or l-phenylephrine significantly ameliorated the decreases in ATP observed in Dbh-/- embryos, suggesting that α- and β-adrenergic receptors were effective modulators of ATP concentrations in mouse embryos in vivo. These data demonstrate that adrenergic hormones stimulate cardiac energy metabolism during a critical period of embryonic development.
MeSH term(s)	Adrenergic Agents/metabolism ; Adrenergic Agents/pharmacology ; Animals ; Autonomic Nervous System Diseases/embryology ; Autonomic Nervous System Diseases/genetics ; Autonomic Nervous System Diseases/metabolism ; Autonomic Nervous System Diseases/physiopathology ; Dopamine beta-Hydroxylase/deficiency ; Dopamine beta-Hydroxylase/genetics ; Dopamine beta-Hydroxylase/metabolism ; Embryo, Mammalian ; Energy Metabolism/drug effects ; Energy Metabolism/genetics ; Epinephrine/metabolism ; Epinephrine/pharmacology ; Female ; Heart/drug effects ; Heart/embryology ; Heart/innervation ; Heart Diseases/embryology ; Heart Diseases/genetics ; Heart Diseases/metabolism ; Isoproterenol/pharmacology ; Maternal-Fetal Exchange/drug effects ; Mice ; Mice, Knockout ; Norepinephrine/deficiency ; Norepinephrine/metabolism ; Norepinephrine/pharmacology ; Pregnancy ; Up-Regulation/drug effects
Chemical Substances	Adrenergic Agents ; Dopamine beta-Hydroxylase (EC 1.14.17.1) ; Isoproterenol (L628TT009W) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2014-12-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00267.2014
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