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Article: Editorial: Mitochondria at the nexus of metabolism, aging, and disease.

Mallilankaraman, Karthik Babu / Kennedy, Brian K / Sorrentino, Vincenzo / Luciani, Alessandro

Frontiers in cell and developmental biology

2024 Volume 11, Page(s) 1356278

Language	English
Publishing date	2024-01-11
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1356278
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Article ; Online: Increased Akt-Driven Glycolysis Is the Basis for the Higher Potency of CD137L-DCs.

Zeng, Qun / Mallilankaraman, Karthik / Schwarz, Herbert

Frontiers in immunology

2019 Volume 10, Page(s) 868

Abstract: CD137 ligand-induced dendritic cells (CD137L-DCs) are a new type of dendritic cells (DCs) that induce strong cytotoxic T cell responses. Investigating the metabolic activity as a potential contributing factor for their potency, we find a significantly ... ...

Abstract	CD137 ligand-induced dendritic cells (CD137L-DCs) are a new type of dendritic cells (DCs) that induce strong cytotoxic T cell responses. Investigating the metabolic activity as a potential contributing factor for their potency, we find a significantly higher rate of glycolysis in CD137L-DCs than in granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin 4 induced monocyte-derived DCs (moDCs). Using unbiased screening, Akt-mTORC1 activity was found to be significantly higher throughout the differentiation and maturation of CD137L-DCs than that of moDCs. Furthermore, this higher activity of the Akt-mTORC1 pathway is responsible for the significantly higher glycolysis rate in CD137L-DCs than in moDCs. Inhibition of Akt during maturation or inhibition of glycolysis during and after maturation resulted in suppression of inflammatory DCs, with mature CD137L-DCs being the most affected ones. mTORC1, instead, was indispensable for the differentiation of both CD137L-DCs and moDCs. In contrast to its role in supporting lipid synthesis in murine bone marrow-derived DCs (BMDCs), the higher glycolysis rate in CD137L-DCs does not lead to a higher lipid content but rather to an accumulation of succinate and serine. These data demonstrate that the increased Akt-driven glycolysis underlies the higher activity of CD137L-DCs.
MeSH term(s)	4-1BB Ligand/metabolism ; Animals ; Cell Differentiation ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Glycolysis ; Humans ; Immunophenotyping ; Lipid Metabolism ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Metabolome ; Metabolomics/methods ; Mice ; Models, Biological ; Proto-Oncogene Proteins c-akt/metabolism ; Serine/metabolism ; Signal Transduction ; Succinic Acid/metabolism
Chemical Substances	4-1BB Ligand ; Serine (452VLY9402) ; Succinic Acid (AB6MNQ6J6L) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2019-04-24
Publishing country	Switzerland
Document type	Journal Article ; 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.2019.00868
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Article: miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A.

Gupta, Neelima / Jadhav, Shweta / Tan, Kai-Leng / Saw, Genevieve / Mallilankaraman, Karthik Babu / Dheen, S Thameem

Frontiers in cellular neuroscience

2020 Volume 14, Page(s) 132

Abstract: Microglia, the innate immune effector cells of the mammalian central nervous system (CNS), are involved in the development, homeostasis, and pathology of CNS. Microglia become activated in response to various insults and injuries and protect the CNS by ... ...

Abstract	Microglia, the innate immune effector cells of the mammalian central nervous system (CNS), are involved in the development, homeostasis, and pathology of CNS. Microglia become activated in response to various insults and injuries and protect the CNS by phagocytosing the invading pathogens, dead neurons, and other cellular debris. Recent studies have demonstrated that the epigenetic mechanisms ensure the coordinated regulation of genes involved in microglial activation. In this study, we performed a microRNA (miRNA) microarray in activated primary microglia derived from rat pup's brain and identified differentially expressed miRNAs targeting key genes involved in cell survival, apoptosis, and inflammatory responses. Interestingly, miR-142-3p, one of the highly up-regulated miRNAs in microglia upon lipopolysaccharide (LPS)-mediated activation, compared to untreated primary microglia cells was predicted to target Ca
Language	English
Publishing date	2020-05-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2020.00132
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Article: Oxygen Glucose Deprivation Induced Prosurvival Autophagy Is Insufficient to Rescue Endothelial Function.

Natarajan, Venkateswaran / Mah, Tania / Peishi, Chen / Tan, Shu Yi / Chawla, Ritu / Arumugam, Thiruma Valavan / Ramasamy, Adaikalavan / Mallilankaraman, Karthik

Frontiers in physiology

2020 Volume 11, Page(s) 533683

Abstract: Endothelial dysfunction, referring to a disturbance in the vascular homeostasis, has been implicated in many disease conditions including ischemic/reperfusion injury and atherosclerosis. Endothelial mitochondria have been increasingly recognized as a ... ...

Abstract	Endothelial dysfunction, referring to a disturbance in the vascular homeostasis, has been implicated in many disease conditions including ischemic/reperfusion injury and atherosclerosis. Endothelial mitochondria have been increasingly recognized as a regulator of calcium homeostasis which has implications in the execution of diverse cellular events and energy production. The mitochondrial calcium uniporter complex through which calcium enters the mitochondria is composed of several proteins, including the pore-forming subunit MCU and its regulators MCUR1, MICU1, and MICU2. Mitochondrial calcium overload leads to opening of MPTP (mitochondrial permeability transition pore) and results in apoptotic cell death. Whereas, blockage of calcium entry into the mitochondria results in reduced ATP production thereby activates AMPK-mediated pro-survival autophagy. Here, we investigated the expression of mitochondrial calcium uniporter complex components (MCU, MCUR1, MICU1, and MICU2), induction of autophagy and apoptotic cell death in endothelial cells in response to oxygen-glucose deprivation. Human pulmonary microvascular endothelial cells (HPMVECs) were subjected to oxygen-glucose deprivation (OGD) at 3-h timepoints up to 12 h. Interestingly, except MCUR1 which was significantly downregulated, all other components of the uniporter (MCU, MICU1, and MICU2) remained unchanged. MCUR1 downregulation has been shown to activate AMPK mediated pro-survival autophagy. Similarly, MCUR1 downregulation in response to OGD resulted in AMPK phosphorylation and LC3 processing indicating the activation of pro-survival autophagy. Despite the activation of autophagy, OGD induced Caspase-mediated apoptotic cell death. Blockade of autophagy did not reduce OGD-induced apoptotic cell death whereas serum starvation conferred enough cellular and functional protection. In conclusion, the autophagic flux induced by MCUR1 downregulation in response to OGD is insufficient in protecting endothelial cells from undergoing apoptotic cell death and requires enhancement of autophagic flux by additional means such as serum starvation.
Language	English
Publishing date	2020-09-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2020.533683
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Article ; Online: Mitochondrial Dysfunction in Age-Related Metabolic Disorders.

Natarajan, Venkateswaran / Chawla, Ritu / Mah, Tania / Vivekanandan, Rajesh / Tan, Shu Yi / Sato, Priscila Y / Mallilankaraman, Karthik

Proteomics

2020 Volume 20, Issue 5-6, Page(s) e1800404

Abstract: Aging is a natural biological process in living organisms characterized by receding bioenergetics. Mitochondria are crucial for cellular bioenergetics and thus an important contributor to age-related energetics deterioration. In addition, mitochondria ... ...

Abstract	Aging is a natural biological process in living organisms characterized by receding bioenergetics. Mitochondria are crucial for cellular bioenergetics and thus an important contributor to age-related energetics deterioration. In addition, mitochondria play a major role in calcium signaling, redox homeostasis, and thermogenesis making this organelle a major cellular component that dictates the fate of a cell. To maintain its quantity and quality, mitochondria undergo multiple processes such as fission, fusion, and mitophagy to eliminate or replace damaged mitochondria. While this bioenergetics machinery is properly protected, the functional decline associated with age and age-related metabolic diseases is mostly a result of failure in such protective mechanisms. In addition, metabolic by-products like reactive oxygen species also aid in this destructive pathway. Mitochondrial dysfunction has always been thought to be associated with diseases. Moreover, studies in recent years have pointed out that aging contributes to the decay of mitochondrial health by promoting imbalances in key mitochondrial-regulated pathways. Hence, it is crucial to understand the nexus of mitochondrial dysfunction in age-related diseases. This review focuses on various aspects of basic mitochondrial biology and its status in aging and age-related metabolic diseases.
MeSH term(s)	Aging ; Animals ; Energy Metabolism ; Humans ; Metabolic Diseases/etiology ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Mitochondria/metabolism ; Mitochondria/pathology ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2020-03-17
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2032093-0
ISSN	1615-9861 ; 1615-9853
ISSN (online)	1615-9861
ISSN	1615-9853
DOI	10.1002/pmic.201800404
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Zs.A 5386: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.A 1868: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Negative Conditioning of Mitochondrial Dysfunction in Age-related Neurodegenerative Diseases.

Selvaraji, Sharmelee / Poh, Luting / Natarajan, Venkateswaran / Mallilankaraman, Karthik / Arumugam, Thiruma V

Conditioning medicine

2018 Volume 2, Issue 1, Page(s) 30–39

Abstract: Mitochondrial dysfunction is regarded as one of the major causes of neuronal injury in age-associated neurodegenerative diseases and stroke. Mitochondrial dysfunction leads to increased reactive oxygen species production, causing mitochondrial DNA ... ...

Abstract	Mitochondrial dysfunction is regarded as one of the major causes of neuronal injury in age-associated neurodegenerative diseases and stroke. Mitochondrial dysfunction leads to increased reactive oxygen species production, causing mitochondrial DNA mutations, which then results in pathological conditions. Negative conditioning of mitochondrial dysfunction via pharmacological inhibition, phytochemicals, and dietary restriction serve as an avenue for therapeutic intervention to improve mitochondrial quality and function. Here, we focus primarily on mitochondrial biology, evidence for mitochondrial dysfunction in neurodegenerative conditions such as dementia and stroke, and the possibility of using negative conditioning to restore or preserve mitochondrial function in these diseases.
Language	English
Publishing date	2018-05-29
Publishing country	United States
Document type	Journal Article
ISSN	2577-3240
ISSN (online)	2577-3240
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Article ; Online: Epigenetic regulation of microglial phosphatidylinositol 3-kinase pathway involved in long-term potentiation and synaptic plasticity in rats.

Saw, Genevieve / Krishna, Kumar / Gupta, Neelima / Soong, Tuck Wah / Mallilankaraman, Karthik / Sajikumar, Sreedharan / Dheen, S Thameem

Glia

2019 Volume 68, Issue 3, Page(s) 656–669

Abstract: Microglia are the main form of immune defense in the central nervous system. Microglia express phosphatidylinositol 3-kinase (PI3K), which has been shown to play a significant role in synaptic plasticity in neurons and inflammation via microglia. This ... ...

Abstract	Microglia are the main form of immune defense in the central nervous system. Microglia express phosphatidylinositol 3-kinase (PI3K), which has been shown to play a significant role in synaptic plasticity in neurons and inflammation via microglia. This study shows that microglial PI3K is regulated epigenetically through histone modifications and posttranslationally through sumoylation and is involved in long-term potentiation (LTP) by modulating the expression of brain-derived neurotrophic factor (BDNF), which has been shown to be involved in neuronal synaptic plasticity. Sodium butyrate, a histone deacetylase inhibitor, upregulates PI3K expression, the phosphorylation of its downstream effectors, AKT and cAMP response element-binding protein (CREB), and the expression of BDNF in microglia, suggesting that BDNF secretion is regulated in microglia via epigenetic regulation of PI3K. Further, knockdown of SUMO1 in BV2 microglia results in a decrease in the expression of PI3K, the phosphorylation of AKT and CREB, as well as the expression of BDNF. These results suggest that microglial PI3K is epigenetically regulated by histone modifications and posttranslationally modified by sumoylation, leading to altered expression of BDNF. Whole-cell voltage-clamp showed the involvement of microglia in neuronal LTP, as selective ablation or disruption of microglia with clodronate in rat hippocampal slices abolished LTP. However, LTP was rescued when the same hippocampal slices were treated with active PI3K or BDNF, indicating that microglial PI3K/AKT signaling contributes to LTP and synaptic plasticity. Understanding the mechanisms by which microglial PI3K influences synapses provides insights into the ways it can modulate synaptic transmission and plasticity in learning and memory.
MeSH term(s)	Animals ; Epigenesis, Genetic ; Hippocampus/metabolism ; Long-Term Potentiation/physiology ; Memory/physiology ; Microglia/metabolism ; Neuronal Plasticity/physiology ; Neurons/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Rats ; Signal Transduction/physiology ; Synapses/metabolism
Language	English
Publishing date	2019-11-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23748
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Zs.A 2345: Show issues

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Article ; Online: Interplay between Notch and p53 promotes neuronal cell death in ischemic stroke.

Balaganapathy, Priyanka / Baik, Sang-Ha / Mallilankaraman, Karthik / Sobey, Christopher G / Jo, Dong-Gyu / Arumugam, Thiruma V

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2017 Volume 38, Issue 10, Page(s) 1781–1795

Abstract: Stroke is the world's second leading cause of mortality, with a high incidence of morbidity. Numerous neuronal membrane receptors are activated by endogenous ligands and may contribute to infarct development. Notch is a well-characterized membrane ... ...

Abstract	Stroke is the world's second leading cause of mortality, with a high incidence of morbidity. Numerous neuronal membrane receptors are activated by endogenous ligands and may contribute to infarct development. Notch is a well-characterized membrane receptor involved in cell differentiation and proliferation, and now shown to play a pivotal role in cell death during ischemic stroke. Blockade of Notch signaling by inhibition of γ-secretase, an enzyme that generates the active form of Notch, is neuroprotective following stroke. We have also identified that Pin1, a peptidyl-prolyl isomerase that regulates p53 transactivation under stress, promotes the pathogenesis of ischemic stroke via Notch signaling. Moreover, Notch can also mediate cell death through a p53-dependent pathway, resulting in apoptosis of neural progenitor cells. The current study has investigated the interplay between Notch and p53 under ischemic stroke conditions. Using pharmacological inhibitors, we have demonstrated that a Notch intracellular domain (NICD)/p53 interaction is involved in transcriptional regulation of genes downstream of p53 and NICD to modify stroke severity. Furthermore, the NICD/p53 interaction confers stability to p53 by rescuing it from ubiquitination. Together, these results indicate that Notch contributes to the pathogenesis of ischemic stroke by promoting p53 stability and signaling.
MeSH term(s)	Animals ; Apoptosis/physiology ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Gene Expression Regulation/physiology ; HEK293 Cells ; Humans ; Mice ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Neurons/metabolism ; Neurons/pathology ; Receptors, Notch/metabolism ; Signal Transduction/physiology ; Stroke/metabolism ; Stroke/pathology ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Receptors, Notch ; Tumor Suppressor Protein p53
Language	English
Publishing date	2017-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X17715956
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Article ; Online: ER-luminal [Ca

Vais, Horia / Wang, Min / Mallilankaraman, Karthik / Payne, Riley / McKennan, Chris / Lock, Jeffrey T / Spruce, Lynn A / Fiest, Carly / Chan, Matthew Yan-Lok / Parker, Ian / Seeholzer, Steven H / Foskett, J Kevin / Mak, Don-On Daniel

eLife

2020 Volume 9

Abstract: Modulating cytoplasmic ... ...

Abstract	Modulating cytoplasmic Ca
MeSH term(s)	A549 Cells ; Animals ; Annexin A1/metabolism ; Calcium/metabolism ; Calcium Signaling/physiology ; Calcium-Binding Proteins/metabolism ; Cell Line, Tumor ; Cell Physiological Phenomena/physiology ; Chickens ; Endoplasmic Reticulum/metabolism ; HEK293 Cells ; Humans ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Ion Channel Gating ; Mice ; Patch-Clamp Techniques ; Rats
Chemical Substances	Annexin A1 ; Calcium-Binding Proteins ; Inositol 1,4,5-Trisphosphate Receptors ; Inositol 1,4,5-Trisphosphate (85166-31-0) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-05-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.53531
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Article ; Online: MCUR1, CCDC90A, Is a Regulator of the Mitochondrial Calcium Uniporter.

Vais, Horia / Tanis, Jessica E / Müller, Marioly / Payne, Riley / Mallilankaraman, Karthik / Foskett, J Kevin

Cell metabolism

2015 Volume 22, Issue 4, Page(s) 533–535

MeSH term(s)	Calcium Channels/metabolism ; Humans ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism
Chemical Substances	Calcium Channels ; Membrane Proteins ; Mitochondrial Proteins
Language	English
Publishing date	2015-10-06
Publishing country	United States
Document type	Comment ; Letter ; Research Support, N.I.H., Extramural
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2015.09.015
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