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Article ; Online: Viability of HepG2 and MCF-7 cells is not correlated with mitochondrial bioenergetics.

Doczi, Judit / Karnok, Noemi / Bui, David / Azarov, Victoria / Pallag, Gergely / Nazarian, Sara / Czumbel, Bence / Seyfried, Thomas N / Chinopoulos, Christos

Scientific reports

2023 Volume 13, Issue 1, Page(s) 10822

Abstract: Alterations in metabolism are a hallmark of cancer. It is unclear if oxidative phosphorylation (OXPHOS) is necessary for tumour cell survival. In this study, we investigated the effects of severe hypoxia, site-specific inhibition of respiratory chain (RC) ...

Abstract	Alterations in metabolism are a hallmark of cancer. It is unclear if oxidative phosphorylation (OXPHOS) is necessary for tumour cell survival. In this study, we investigated the effects of severe hypoxia, site-specific inhibition of respiratory chain (RC) components, and uncouplers on necrotic and apoptotic markers in 2D-cultured HepG2 and MCF-7 tumour cells. Comparable respiratory complex activities were observed in both cell lines. However, HepG2 cells exhibited significantly higher oxygen consumption rates (OCR) and respiratory capacity than MCF-7 cells. Significant non-mitochondrial OCR was observed in MCF-7 cells, which was insensitive to acute combined inhibition of complexes I and III. Pre-treatment of either cell line with RC inhibitors for 24-72 h resulted in the complete abolition of respective complex activities and OCRs. This was accompanied by a time-dependent decrease in citrate synthase activity, suggesting mitophagy. High-content automated microscopy recordings revealed that the viability of HepG2 cells was mostly unaffected by any pharmacological treatment or severe hypoxia. In contrast, the viability of MCF-7 cells was strongly affected by inhibition of complex IV (CIV) or complex V (CV), severe hypoxia, and uncoupling. However, it was only moderately affected by inhibition of complexes I, II, and III. Cell death in MCF-7 cells induced by inhibition of complexes II, III, and IV was partially abrogated by aspartate. These findings indicate that OXPHOS activity and viability are not correlated in these cell lines, suggesting that the connection between OXPHOS and cancer cell survival is dependent on the specific cell type and conditions.
MeSH term(s)	Humans ; MCF-7 Cells ; Energy Metabolism ; Mitochondria/metabolism ; Oxidative Phosphorylation ; Electron Transport Complex I/metabolism ; Hypoxia/metabolism
Chemical Substances	Electron Transport Complex I (EC 7.1.1.2)
Language	English
Publishing date	2023-07-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-37677-x
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Article: Bridging the Gap: Multi-Omics Profiling of Brain Tissue in Alzheimer's Disease and Older Controls in Multi-Ethnic Populations.

Reddy, Joseph S / Heath, Laura / Linden, Abby Vander / Allen, Mariet / de Paiva Lopes, Katia / Seifar, Fatemeh / Wang, Erming / Ma, Yiyi / Poehlman, William L / Quicksall, Zachary S / Runnels, Alexi / Wang, Yanling / Duong, Duc M / Yin, Luming / Xu, Kaiming / Modeste, Erica S / Shantaraman, Anantharaman / Dammer, Eric B / Ping, Lingyan /

Oatman, Stephanie R / Scanlan, Jo / Ho, Charlotte / Carrasquillo, Minerva M / Atik, Merve / Yepez, Geovanna / Mitchell, Adriana O / Nguyen, Thuy T / Chen, Xianfeng / Marquez, David X / Reddy, Hasini / Xiao, Harrison / Seshadri, Sudha / Mayeux, Richard / Prokop, Stefan / Lee, Edward B / Serrano, Geidy E / Beach, Thomas G / Teich, Andrew F / Haroutunian, Varham / Fox, Edward J / Gearing, Marla / Wingo, Aliza / Wingo, Thomas / Lah, James J / Levey, Allan I / Dickson, Dennis W / Barnes, Lisa L / De Jager, Philip / Zhang, Bin / Bennett, David / Seyfried, Nicholas T / Greenwood, Anna K / Ertekin-Taner, Nilüfer

bioRxiv : the preprint server for biology

2024

Abstract: ... from AA (n=306), LA (n=326), or AA : Discussion: Inclusion of traditionally underrepresented groups ...

Abstract	Introduction: Multi-omics studies in Alzheimer's disease (AD) revealed many potential disease pathways and therapeutic targets. Despite their promise of precision medicine, these studies lacked African Americans (AA) and Latin Americans (LA), who are disproportionately affected by AD. Methods: To bridge this gap, Accelerating Medicines Partnership in AD (AMP-AD) expanded brain multi-omics profiling to multi-ethnic donors. Results: We generated multi-omics data and curated and harmonized phenotypic data from AA (n=306), LA (n=326), or AA Discussion: Inclusion of traditionally underrepresented groups in multi-omics studies is essential to discover the full spectrum of precision medicine targets that will be pertinent to all populations affected with AD.
Language	English
Publishing date	2024-04-20
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.16.589592
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Article ; Online: Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia.

Scientific reports

2024 Volume 14, Issue 1, Page(s) 1729

Abstract: Anoxia halts oxidative phosphorylation (OXPHOS) causing an accumulation of reduced compounds in the mitochondrial matrix which impedes dehydrogenases. By simultaneously measuring oxygen concentration, NADH autofluorescence, mitochondrial membrane ... ...

Abstract	Anoxia halts oxidative phosphorylation (OXPHOS) causing an accumulation of reduced compounds in the mitochondrial matrix which impedes dehydrogenases. By simultaneously measuring oxygen concentration, NADH autofluorescence, mitochondrial membrane potential and ubiquinone reduction extent in isolated mitochondria in real-time, we demonstrate that Complex I utilized endogenous quinones to oxidize NADH under acute anoxia.
MeSH term(s)	Humans ; NAD/metabolism ; Mitochondria/metabolism ; Electron Transport Complex I/metabolism ; Quinones/metabolism ; Oxidative Phosphorylation ; Succinates/metabolism ; Hypoxia/metabolism ; Oxidation-Reduction
Chemical Substances	NAD (0U46U6E8UK) ; Electron Transport Complex I (EC 7.1.1.2) ; Quinones ; Succinates
Language	English
Publishing date	2024-01-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-51365-4
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Article ; Online: Chemical mutagenesis of a GPCR ligand: Detoxifying "inflammo-attraction" to direct therapeutic stem cell migration.

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 49, Page(s) 31177–31188

Abstract: A transplanted stem cell's engagement with a pathologic niche is the first step in its restoring homeostasis to that site. Inflammatory chemokines are constitutively produced in such a niche; their binding to receptors on the stem cell helps direct that ... ...

Abstract	A transplanted stem cell's engagement with a pathologic niche is the first step in its restoring homeostasis to that site. Inflammatory chemokines are constitutively produced in such a niche; their binding to receptors on the stem cell helps direct that cell's "pathotropism." Neural stem cells (NSCs), which express CXCR4, migrate to sites of CNS injury or degeneration in part because astrocytes and vasculature produce the inflammatory chemokine CXCL12. Binding of CXCL12 to CXCR4 (a G protein-coupled receptor, GPCR) triggers repair processes within the NSC. Although a tool directing NSCs to where needed has been long-sought, one would not inject this chemokine in vivo because undesirable inflammation also follows CXCL12-CXCR4 coupling. Alternatively, we chemically "mutated" CXCL12, creating a CXCR4 agonist that contained a strong pure binding motif linked to a signaling motif devoid of sequences responsible for synthetic functions. This synthetic dual-moity CXCR4 agonist not only elicited more extensive and persistent human NSC migration and distribution than did native CXCL 12, but induced no host inflammation (or other adverse effects); rather, there was predominantly reparative gene expression. When co-administered with transplanted human induced pluripotent stem cell-derived hNSCs in a mouse model of a prototypical neurodegenerative disease, the agonist enhanced migration, dissemination, and integration of donor-derived cells into the diseased cerebral cortex (including as electrophysiologically-active cortical neurons) where their secreted cross-corrective enzyme mediated a therapeutic impact unachieved by cells alone. Such a "designer" cytokine receptor-agonist peptide illustrates that treatments can be controlled and optimized by exploiting fundamental stem cell properties (e.g., "inflammo-attraction").
MeSH term(s)	Astrocytes/metabolism ; Astrocytes/pathology ; Cell Movement/genetics ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Chemokine CXCL12/genetics ; Humans ; Induced Pluripotent Stem Cells ; Inflammation/genetics ; Ligands ; Mutagenesis/genetics ; Neural Stem Cells/metabolism ; Neural Stem Cells/transplantation ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/therapy ; Neurons/metabolism ; Neurons/pathology ; Protein Binding/genetics ; Receptors, CXCR4/genetics
Chemical Substances	CXCR4 protein, human ; Chemokine CXCL12 ; Ligands ; Receptors, CXCR4
Language	English
Publishing date	2020-11-20
Publishing country	United States
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	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1911444117
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Article ; Online: Targeting energy metabolism in brain cancer through calorie restriction and the ketogenic diet.

Seyfried, B Thomas N / Kiebish, Michael / Marsh, Jeremy / Mukherjee, Purna

Journal of cancer research and therapeutics

2009 Volume 5 Suppl 1, Page(s) S7–15

Abstract: Malignant brain tumors are a significant health problem in children and adults and are largely unmanageable. As a metabolic disorder involving the dysregulation of glycolysis and respiration (the Warburg effect), malignant brain cancer can be managed ... ...

Abstract	Malignant brain tumors are a significant health problem in children and adults and are largely unmanageable. As a metabolic disorder involving the dysregulation of glycolysis and respiration (the Warburg effect), malignant brain cancer can be managed through changes in metabolic environment. In contrast to malignant brain tumors that are mostly dependent on glycolysis for energy, normal neurons and glia readily transition to ketone bodies (beta-hydroxybutyrate) for energy in vivo when glucose levels are reduced. The transition from glucose to ketone bodies as a major energy source is an evolutionary conserved adaptation to food deprivation that permits the survival of normal cells during extreme shifts in nutritional environment. Only those cells with a flexible genome, honed through millions of years of environmental forcing and variability selection, can transition from one energy state to another. We propose a different approach to brain cancer management that exploits the metabolic flexibility of normal cells at the expense of the genetically defective and less metabolically flexible tumor cells. This approach to brain cancer management is supported from recent studies in orthotopic mouse brain tumor models and in human pediatric astrocytoma treated with calorie restriction and the ketogenic diet. Issues of implementation and use protocols are discussed.
MeSH term(s)	Animals ; Brain Neoplasms/metabolism ; Caloric Restriction ; Diet, Ketogenic ; Energy Metabolism/physiology ; Humans
Language	English
Publishing date	2009-09
Publishing country	India
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2187633-2
ISSN	1998-4138 ; 0973-1482
ISSN (online)	1998-4138
ISSN	0973-1482
DOI	10.4103/0973-1482.55134
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Article ; Online: Caloric restriction in C57BL/6J mice mimics therapeutic fasting in humans.

Mahoney, Lisa B / Denny, Christine A / Seyfried, Thomas N

Lipids in health and disease

2006 Volume 5, Page(s) 13

Abstract: ... humans.: Results: Three groups of individually housed adult female C57BL/6J (B6) mice (n = 4/group ...

Abstract	Background: Caloric restriction (CR) has long been recognized as a dietary therapy that improves health and increases longevity. Little is known about the persistent effects of CR on plasma biomarkers (glucose, ketone bodies, and lipids) following re-feeding in mice. It is also unclear how these biomarker changes in calorically restricted mice relate to those observed previously in calorically restricted humans. Results: Three groups of individually housed adult female C57BL/6J (B6) mice (n = 4/group) were fed a standard rodent chow diet either: (1) unrestricted (UR); (2) restricted for three weeks to reduce body weight by approximately 15-20% (R); or (3) restricted for three weeks and then re-fed unrestricted (ad libitum) for an additional three weeks (R-RF). Body weight and food intake were measured throughout the study, while plasma lipids and levels of glucose and ketone bodies (beta-hydroxybutyrate) were measured at the termination of the study. Plasma glucose, phosphatidylcholine, cholesterol, and triglycerides were significantly lower in the R mice than in the UR mice. In contrast, plasma fatty acids and beta-hydroxybutyrate were significantly higher in the R mice than in the UR mice. CR had no effect on plasma phosphatidylinositol levels. While body weight and plasma lipids of the R-RF mice returned to unrestricted levels upon re-feeding, food intake and glucose levels remained significantly lower than those prior to the initiation of CR. Conclusion: CR establishes a new homeostatic state in B6 mice that persists for at least three weeks following ad libitum re-feeding. Moreover, the plasma biomarker changes observed in B6 mice during CR mimic those reported in humans on very low calorie diets or during therapeutic fasting.
MeSH term(s)	3-Hydroxybutyric Acid/blood ; Animals ; Biomarkers/blood ; Blood Glucose/metabolism ; Body Weight/physiology ; Caloric Restriction ; Cholesterol/blood ; Eating/physiology ; Fasting/blood ; Female ; Homeostasis/physiology ; Humans ; Lipids/blood ; Mice ; Mice, Inbred C57BL ; Phosphatidylcholines/blood ; Triglycerides/blood
Chemical Substances	Biomarkers ; Blood Glucose ; Lipids ; Phosphatidylcholines ; Triglycerides ; Cholesterol (97C5T2UQ7J) ; 3-Hydroxybutyric Acid (TZP1275679)
Language	English
Publishing date	2006-05-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1476-511X
ISSN (online)	1476-511X
DOI	10.1186/1476-511X-5-13
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Article: Predictors of Cognitive Decline in Healthy Middle-Aged Individuals with Asymptomatic Alzheimer's Disease.

Research square

2023

Abstract: ... N=1149) in the Emory Healthy Brain Study were assayed for Aβ ...

Abstract	Alzheimer's disease (AD) progresses through a lengthy asymptomatic period during which pathological changes accumulate prior to development of clinical symptoms. As disease-modifying treatments are developed, tools to stratify risk of clinical disease will be required to guide their use. In this study, we examine the relationship of AD biomarkers in healthy middle-aged individuals to health history, family history, and neuropsychological measures and identify cerebrospinal fluid (CSF) biomarkers to stratify risk of progression from asymptomatic to symptomatic AD. CSF from cognitively normal (CN) individuals (N=1149) in the Emory Healthy Brain Study were assayed for Aβ
Language	English
Publishing date	2023-02-28
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-2577025/v1
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Article: Aβ Amyloid Scaffolds the Accumulation of Matrisome and Additional Proteins in Alzheimer's Disease.

Levites, Yona / Dammer, Eric B / Ran, Yong / Tsering, Wangchen / Duong, Duc / Abreha, Measho / Gadhavi, Joshna / Lolo, Kiara / Trejo-Lopez, Jorge / Phillips, Jennifer L / Iturbe, Andrea / Erqiuzi, Aya / Moore, Brenda Dawn / Ryu, Danny / Natu, Aditya / Dillon, Kristy D / Torrellas, Jose / Moran, Corey / Ladd, Thomas B /

Afroz, Kazi Farhana / Islam, Tariful / Jagirdar, Jaishree / Funk, Cory C / Robinson, Max / Borchelt, David R / Ertekin-Taner, Nilufer / Kelly, Jeffrey W / Heppner, Frank L / Johnson, Erik Cb / McFarland, Karen / Levey, Allan L / Prokop, Stefan / Seyfried, Nicholas T / Golde, Todd E

bioRxiv : the preprint server for biology

2023

Abstract: We report a highly significant correlation in brain proteome changes between Alzheimers disease (AD) and CRND8 APP695NL/F transgenic mice. However, integrating protein changes observed in the CRND8 mice with co-expression networks derived from human AD, ... ...

Abstract	We report a highly significant correlation in brain proteome changes between Alzheimers disease (AD) and CRND8 APP695NL/F transgenic mice. However, integrating protein changes observed in the CRND8 mice with co-expression networks derived from human AD, reveals both conserved and divergent module changes. For the most highly conserved module (M42, matrisome) we find many proteins accumulate in plaques, cerebrovascular amyloid (CAA), dystrophic processes, or a combination thereof. Overexpression of two M42 proteins, midkine (Mdk) and pleiotrophin (PTN), in CRND8 mice brains leads to increased accumulation of A β in plaques and in CAA; further, recombinant MDK and PTN enhance A β aggregation into amyloid. Multiple M42 proteins, annotated as heparan sulfate binding proteins, bind to fibrillar A β 42 and a non-human amyloid fibril in vitro. Supporting this binding data, MDK and PTN co-accumulate with transthyretin (TTR) amyloid in the heart and islet amyloid polypeptide (IAPP) amyloid in the pancreas. Our findings establish several critical insights. Proteomic changes in modules observed in human AD brains define an A β amyloid responsome that is well conserved from mouse model to human. Further, distinct amyloid structures may serve as scaffolds, facilitating the co-accumulation of proteins with signaling functions. We hypothesize that this co-accumulation may contribute to downstream pathological sequalae. Overall, this contextualized understanding of proteomic changes and their interplay with amyloid deposition provides valuable insights into the complexity of AD pathogenesis and potential biomarkers and therapeutic targets.
Language	English
Publishing date	2023-12-07
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.29.568318
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Article ; Online: APOE expression and secretion are modulated by mitochondrial dysfunction.

Wynne, Meghan E / Ogunbona, Oluwaseun / Lane, Alicia R / Gokhale, Avanti / Zlatic, Stephanie A / Xu, Chongchong / Wen, Zhexing / Duong, Duc M / Rayaprolu, Sruti / Ivanova, Anna / Ortlund, Eric A / Dammer, Eric B / Seyfried, Nicholas T / Roberts, Blaine R / Crocker, Amanda / Shanbhag, Vinit / Petris, Michael / Senoo, Nanami / Kandasamy, Selvaraju /

Claypool, Steven Michael / Barrientos, Antoni / Wingo, Aliza / Wingo, Thomas S / Rangaraju, Srikant / Levey, Allan I / Werner, Erica / Faundez, Victor

eLife

2023 Volume 12

Abstract: Mitochondria influence cellular function through both cell-autonomous and non-cell autonomous mechanisms, such as production of paracrine and endocrine factors. Here, we demonstrate that mitochondrial regulation of the secretome is more extensive than ... ...

Abstract	Mitochondria influence cellular function through both cell-autonomous and non-cell autonomous mechanisms, such as production of paracrine and endocrine factors. Here, we demonstrate that mitochondrial regulation of the secretome is more extensive than previously appreciated, as both genetic and pharmacological disruption of the electron transport chain caused upregulation of the Alzheimer's disease risk factor apolipoprotein E (APOE) and other secretome components. Indirect disruption of the electron transport chain by gene editing of SLC25A mitochondrial membrane transporters as well as direct genetic and pharmacological disruption of either complexes I, III, or the copper-containing complex IV of the electron transport chain elicited upregulation of APOE transcript, protein, and secretion, up to 49-fold. These APOE phenotypes were robustly expressed in diverse cell types and iPSC-derived human astrocytes as part of an inflammatory gene expression program. Moreover, age- and genotype-dependent decline in brain levels of respiratory complex I preceded an increase in APOE in the 5xFAD mouse model. We propose that mitochondria act as novel upstream regulators of APOE-dependent cellular processes in health and disease.
MeSH term(s)	Animals ; Humans ; Mice ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Astrocytes/metabolism ; Genotype ; Mitochondria/metabolism ; Mitochondria/pathology
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E
Language	English
Publishing date	2023-05-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.85779
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Article ; Online: Therapeutic benefit of combining calorie-restricted ketogenic diet and glutamine targeting in late-stage experimental glioblastoma.

Mukherjee, Purna / Augur, Zachary M / Li, Mingyi / Hill, Collin / Greenwood, Bennett / Domin, Marek A / Kondakci, Gramoz / Narain, Niven R / Kiebish, Michael A / Bronson, Roderick T / Arismendi-Morillo, Gabriel / Chinopoulos, Christos / Seyfried, Thomas N

Communications biology

2019 Volume 2, Page(s) 200

Abstract: Glioblastoma (GBM) is an aggressive primary human brain tumour that has resisted effective therapy for decades. Although glucose and glutamine are the major fuels that drive GBM growth and invasion, few studies have targeted these fuels for therapeutic ... ...

Abstract	Glioblastoma (GBM) is an aggressive primary human brain tumour that has resisted effective therapy for decades. Although glucose and glutamine are the major fuels that drive GBM growth and invasion, few studies have targeted these fuels for therapeutic management. The glutamine antagonist, 6-diazo-5-oxo-L-norleucine (DON), was administered together with a calorically restricted ketogenic diet (KD-R) to treat late-stage orthotopic growth in two syngeneic GBM mouse models: VM-M3 and CT-2A. DON targets glutaminolysis, while the KD-R reduces glucose and, simultaneously, elevates neuroprotective and non-fermentable ketone bodies. The diet/drug therapeutic strategy killed tumour cells while reversing disease symptoms, and improving overall mouse survival. The therapeutic strategy also reduces edema, hemorrhage, and inflammation. Moreover, the KD-R diet facilitated DON delivery to the brain and allowed a lower dosage to achieve therapeutic effect. The findings support the importance of glucose and glutamine in driving GBM growth and provide a therapeutic strategy for non-toxic metabolic management.
MeSH term(s)	Animals ; Body Weight ; Brain/metabolism ; Brain Neoplasms/metabolism ; Brain Neoplasms/therapy ; Caloric Restriction ; Cell Line, Tumor ; Cell Proliferation ; Diazooxonorleucine/therapeutic use ; Diet, Ketogenic ; Disease Models, Animal ; Female ; Fermentation ; Glioblastoma/metabolism ; Glioblastoma/therapy ; Glucose/metabolism ; Glutamine/metabolism ; Humans ; Immunohistochemistry ; Ketone Bodies/metabolism ; Ketones ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation
Chemical Substances	Ketone Bodies ; Ketones ; Diazooxonorleucine (03J0H273KZ) ; Glutamine (0RH81L854J) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-05-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-019-0455-x
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