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Article: LDHB Deficiency Promotes Mitochondrial Dysfunction Mediated Oxidative Stress and Neurodegeneration in Adult Mouse Brain.

Park, Jun Sung / Saeed, Kamran / Jo, Myeung Hoon / Kim, Min Woo / Lee, Hyeon Jin / Park, Chan-Bae / Lee, Gwang / Kim, Myeong Ok

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 2

Abstract: Age-related decline in mitochondrial function and oxidative stress plays a critical role in neurodegeneration. Lactate dehydrogenase-B (LDHB) is a glycolytic enzyme that catalyzes the conversion of lactate, an important brain energy substrate, into ... ...

Abstract	Age-related decline in mitochondrial function and oxidative stress plays a critical role in neurodegeneration. Lactate dehydrogenase-B (LDHB) is a glycolytic enzyme that catalyzes the conversion of lactate, an important brain energy substrate, into pyruvate. It has been reported that the LDHB pattern changes in the brain during ageing. Yet very little is known about the effect of LDHB deficiency on brain pathology. Here, we have used Ldhb knockout (
Language	English
Publishing date	2022-01-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11020261
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Article: The Impact of Fine Particulate Matter 2.5 on the Cardiovascular System: A Review of the Invisible Killer.

Basith, Shaherin / Manavalan, Balachandran / Shin, Tae Hwan / Park, Chan Bae / Lee, Wang-Soo / Kim, Jaetaek / Lee, Gwang

Nanomaterials (Basel, Switzerland)

2022 Volume 12, Issue 15

Abstract: Air pollution exerts several deleterious effects on the cardiovascular system, with cardiovascular disease (CVD) accounting for 80% of all premature deaths caused by air pollution. Short-term exposure to particulate matter 2.5 ( ... ...

Abstract	Air pollution exerts several deleterious effects on the cardiovascular system, with cardiovascular disease (CVD) accounting for 80% of all premature deaths caused by air pollution. Short-term exposure to particulate matter 2.5 (PM
Language	English
Publishing date	2022-08-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662255-5
ISSN	2079-4991
ISSN	2079-4991
DOI	10.3390/nano12152656
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Article: LDHB Deficiency Promotes Mitochondrial Dysfunction Mediated Oxidative Stress and Neurodegeneration in Adult Mouse Brain

Park, Jun Sung / Saeed, Kamran / Jo, Myeung Hoon / Kim, Min Woo / Lee, Hyeon Jin / Park, Chan-Bae / Lee, Gwang / Kim, Myeong Ok

Antioxidants. 2022 Jan. 28, v. 11, no. 2

2022

Abstract	Age-related decline in mitochondrial function and oxidative stress plays a critical role in neurodegeneration. Lactate dehydrogenase-B (LDHB) is a glycolytic enzyme that catalyzes the conversion of lactate, an important brain energy substrate, into pyruvate. It has been reported that the LDHB pattern changes in the brain during ageing. Yet very little is known about the effect of LDHB deficiency on brain pathology. Here, we have used Ldhb knockout (Ldhb⁻/⁻⁾ mice to test the hypothesis that LDHB deficiency plays an important role in oxidative stress-mediated neuroinflammation and neurodegeneration. LDHB knockout (Ldhb⁻/⁻) mice were generated by the ablation of the Ldhb gene using the Cre/loxP-recombination system in the C57BL/6 genetic background. The Ldhb⁻/⁻ mice were treated with either osmotin (15 μg/g of the body; intraperitoneally) or vehicle twice a week for 5-weeks. After behavior assessments, the mice were sacrificed, and the cortical and hippocampal brain regions were analyzed through biochemical and morphological analysis. Ldhb⁻/⁻ mice displayed enhanced reactive oxygen species (ROS) and lipid peroxidation (LPO) production, and they revealed depleted stores of cellular ATP, GSH:GSSG enzyme ratio, and downregulated expression of Nrf2 and HO-1 proteins, when compared to WT littermates. Importantly, the Ldhb⁻/⁻ mice showed upregulated expression of apoptosis mediators (Bax, Cytochrome C, and caspase-3), and revealed impaired p-AMPK/SIRT1/PGC-1alpha signaling. Moreover, LDHB deficiency-induced gliosis increased the production of inflammatory mediators (TNF-α, Nf-ĸB, and NOS2), and revealed cognitive deficits. Treatment with osmotin, an adipoR1 natural agonist, significantly increased cellular ATP production by increasing mitochondrial function and attenuated oxidative stress, neuroinflammation, and neuronal apoptosis, probably, by upregulating p-AMPK/SIRT1/PGC-1alpha signaling in Ldhb⁻/⁻ mice. In brief, LDHB deficiency may lead to brain oxidative stress-mediated progression of neurodegeneration via regulating p-AMPK/SIRT1/PGC-1alpha signaling, while osmotin could improve mitochondrial functions, abrogate oxidative stress and alleviate neuroinflammation and neurodegeneration in adult Ldhb⁻/⁻ mice.
Keywords	adults ; agonists ; apoptosis ; brain ; caspase-3 ; cognition ; cytochrome c ; energy ; genes ; genetic background ; glycolysis ; lactic acid ; lipid peroxidation ; mice ; mitochondria ; neurodegenerative diseases ; neurons ; oxidative stress ; pyruvic acid ; reactive oxygen species
Language	English
Dates of publication	2022-0128
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11020261
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Article: Diesel-derived PM

Shin, Tae Hwan / Kim, Seok Gi / Ji, Moongi / Kwon, Do Hyeon / Hwang, Ji Su / George, Nimisha Pradeep / Ergando, Dube Solomon / Park, Chan Bae / Paik, Man Jeong / Lee, Gwang

Frontiers in endocrinology

2022 Volume 13, Page(s) 999475

Abstract: Particulate matter (PM) in polluted air can be exposed to the human body through inhalation, ingestion, and skin contact, accumulating in various organs throughout the body. Organ accumulation of PM is a growing health concern, particularly in the ... ...

Abstract	Particulate matter (PM) in polluted air can be exposed to the human body through inhalation, ingestion, and skin contact, accumulating in various organs throughout the body. Organ accumulation of PM is a growing health concern, particularly in the cardiovascular system. PM emissions are formed in the air by solid particles, liquid droplets, and fuel - particularly diesel - combustion. PM
MeSH term(s)	Adenosine Triphosphate/analysis ; Adenosine Triphosphate/metabolism ; Adenosine Triphosphate/pharmacology ; Air Pollutants/analysis ; Air Pollutants/toxicity ; Amino Acids/metabolism ; Animals ; Chromatography, Liquid ; Humans ; Mice ; Mitochondria/metabolism ; Myocytes, Cardiac/metabolism ; Particulate Matter/analysis ; Particulate Matter/toxicity ; Reactive Oxygen Species/metabolism ; Tandem Mass Spectrometry
Chemical Substances	Air Pollutants ; Amino Acids ; Particulate Matter ; Reactive Oxygen Species ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2022-09-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2022.999475
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Article ; Online: Mitochondrial DNA mutations in disease and aging.

Park, Chan Bae / Larsson, Nils-Göran

The Journal of cell biology

2011 Volume 193, Issue 5, Page(s) 809–818

Abstract: The small mammalian mitochondrial DNA (mtDNA) is very gene dense and encodes factors critical for oxidative phosphorylation. Mutations of mtDNA cause a variety of human mitochondrial diseases and are also heavily implicated in age-associated disease and ... ...

Abstract	The small mammalian mitochondrial DNA (mtDNA) is very gene dense and encodes factors critical for oxidative phosphorylation. Mutations of mtDNA cause a variety of human mitochondrial diseases and are also heavily implicated in age-associated disease and aging. There has been considerable progress in our understanding of the role for mtDNA mutations in human pathology during the last two decades, but important mechanisms in mitochondrial genetics remain to be explained at the molecular level. In addition, mounting evidence suggests that most mtDNA mutations may be generated by replication errors and not by accumulated damage.
MeSH term(s)	Aging/genetics ; Animals ; DNA Replication/genetics ; DNA, Mitochondrial/genetics ; Disease/genetics ; Humans ; Mutation/genetics
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2011-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201010024
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Article ; Online: High levels of TFAM repress mammalian mitochondrial DNA transcription in vivo.

Bonekamp, Nina A / Jiang, Min / Motori, Elisa / Garcia Villegas, Rodolfo / Koolmeister, Camilla / Atanassov, Ilian / Mesaros, Andrea / Park, Chan Bae / Larsson, Nils-Göran

Life science alliance

2021 Volume 4, Issue 11

Abstract: Mitochondrial transcription factor A (TFAM) is compacting mitochondrial DNA (dmtDNA) into nucleoids and directly controls mtDNA copy number. Here, we show that the TFAM-to-mtDNA ratio is critical for maintaining normal mtDNA expression in different mouse ...

Abstract	Mitochondrial transcription factor A (TFAM) is compacting mitochondrial DNA (dmtDNA) into nucleoids and directly controls mtDNA copy number. Here, we show that the TFAM-to-mtDNA ratio is critical for maintaining normal mtDNA expression in different mouse tissues. Moderately increased TFAM protein levels increase mtDNA copy number but a normal TFAM-to-mtDNA ratio is maintained resulting in unaltered mtDNA expression and normal whole animal metabolism. Mice ubiquitously expressing very high TFAM levels develop pathology leading to deficient oxidative phosphorylation (OXPHOS) and early postnatal lethality. The TFAM-to-mtDNA ratio varies widely between tissues in these mice and is very high in skeletal muscle leading to strong repression of mtDNA expression and OXPHOS deficiency. In the heart, increased mtDNA copy number results in a near normal TFAM-to-mtDNA ratio and maintained OXPHOS capacity. In liver, induction of LONP1 protease and mitochondrial RNA polymerase expression counteracts the silencing effect of high TFAM levels. TFAM thus acts as a general repressor of mtDNA expression and this effect can be counterbalanced by tissue-specific expression of regulatory factors.
MeSH term(s)	Animals ; DNA Replication ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression/genetics ; Gene Expression Regulation/genetics ; High Mobility Group Proteins/genetics ; High Mobility Group Proteins/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Mitochondrial Diseases/genetics ; Mitochondrial Proteins/metabolism ; Oxidation-Reduction ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic
Chemical Substances	DNA, Mitochondrial ; DNA-Binding Proteins ; High Mobility Group Proteins ; Mitochondrial Proteins ; Tfam protein, mouse ; Transcription Factors ; mitochondrial transcription factor A
Language	English
Publishing date	2021-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202101034
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Article ; Online: Expanding the genetic code of Mus musculus.

Han, Songmi / Yang, Aerin / Lee, Soonjang / Lee, Han-Woong / Park, Chan Bae / Park, Hee-Sung

Nature communications

2017 Volume 8, Page(s) 14568

Abstract: Here we report the expansion of the genetic code of Mus musculus with various unnatural amino acids including ... ...

Abstract	Here we report the expansion of the genetic code of Mus musculus with various unnatural amino acids including N
MeSH term(s)	Amino Acids/genetics ; Amino Acyl-tRNA Synthetases/genetics ; Animals ; Codon, Terminator/genetics ; Genetic Code/genetics ; Genetic Engineering/methods ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Lysine/genetics ; Mice, Transgenic ; Microscopy, Fluorescence ; RNA, Transfer/genetics
Chemical Substances	Amino Acids ; Codon, Terminator ; Green Fluorescent Proteins (147336-22-9) ; RNA, Transfer (9014-25-9) ; Amino Acyl-tRNA Synthetases (EC 6.1.1.-) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2017-02-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms14568
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Article: Expression of Cellular Receptors in the Ischemic Hemisphere of Mice with Increased Glucose Uptake.

Lee, Jin Soo / Hong, Ji Man / Yoon, Bok Seon / Son, Keoung Sun / Lee, Kyung Eon / Im, Doo Soon / Park, Bok-Nam / An, Young-Sil / Hwang, Dong Hoon / Park, Chan Bae / Kim, Byung Gon / Joe, Eun-Hye

Experimental neurobiology

2020 Volume 29, Issue 1, Page(s) 70–79

Abstract: Many previous studies have shown reduced glucose uptake in the ischemic brain. In contrast, in a permanent unilateral common carotid artery occlusion (UCCAO) mouse model, our pilot experiments using 18F-fluorodeoxyglucose positron emission tomography ( ... ...

Abstract	Many previous studies have shown reduced glucose uptake in the ischemic brain. In contrast, in a permanent unilateral common carotid artery occlusion (UCCAO) mouse model, our pilot experiments using 18F-fluorodeoxyglucose positron emission tomography (FDG PET) revealed that a subset of mice exhibited conspicuously high uptake of glucose in the ipsilateral hemisphere at 1 week post-occlusion (asymmetric group), whereas other mice showed symmetric uptake in both hemispheres (symmetric group). Thus, we aimed to understand the discrepancy between the two groups. Cerebral blood flow and histological/metabolic changes were analyzed using laser Doppler flowmetry and immunohistochemistry/Western blotting, respectively. Contrary to the increased glucose uptake observed in the ischemic cerebral hemisphere on FDG PET (p<0.001), cerebral blood flow tended to be lower in the asymmetric group than in the symmetric group (right to left ratio [%], 36.4±21.8 vs. 58.0±24.8, p=0.059). Neuronal death was observed only in the ischemic hemisphere of the asymmetric group. In contrast, astrocytes were more activated in the asymmetric group than in the symmetric group (p<0.05). Glucose transporter-1, and monocarboxylate transporter-1 were also upregulated in the asymmetric group, compared with the symmetric group (p<0.05, respectively). These results suggest that the increased FDG uptake was associated with relatively severe ischemia, and glucose transporter-1 upregulation and astrocyte activation. Glucose metabolism may thus be a compensatory mechanism in the moderately severe ischemic brain.
Language	English
Publishing date	2020-03-02
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2639017-6
ISSN	2093-8144 ; 1226-2560
ISSN (online)	2093-8144
ISSN	1226-2560
DOI	10.5607/en.2020.29.1.70
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Article ; Online: Suppressed expression of LDHB promotes age-related hearing loss via aerobic glycolysis.

Tian, Chunjie / Kim, Yeon Ju / Hali, Sai / Choo, Oak-Sung / Lee, Jin-Sol / Jung, Seo-Kyung / Choi, Youn-Uk / Park, Chan Bae / Choung, Yun-Hoon

Cell death & disease

2020 Volume 11, Issue 5, Page(s) 375

Abstract: Age-dependent decrease of mitochondrial energy production and cellular redox imbalance play significant roles in age-related hearing loss (ARHL). Lactate dehydrogenase B (LDHB) is a key glycolytic enzyme that catalyzes the interconversion of pyruvate and ...

Abstract	Age-dependent decrease of mitochondrial energy production and cellular redox imbalance play significant roles in age-related hearing loss (ARHL). Lactate dehydrogenase B (LDHB) is a key glycolytic enzyme that catalyzes the interconversion of pyruvate and lactate. LDH activity and isoenzyme patterns are known to be changed with aging, but the role of LDHB in ARHL has not been studied yet. Here, we found that LDHB knockout mice showed hearing loss at high frequencies, which is the typical feature of ARHL. LDHB knockdown caused downregulation of mitochondrial functions in auditory cell line, University of Bristol/organ of Corti 1 (UB/OC1) with decreased NAD
MeSH term(s)	Age Factors ; Animals ; Cell Line, Tumor ; Glycolysis/physiology ; Hearing Loss/metabolism ; Hearing Loss/physiopathology ; Isoenzymes/metabolism ; L-Lactate Dehydrogenase/metabolism ; Lactic Acid/metabolism ; Mice ; Mitochondria/metabolism ; Pyruvic Acid/metabolism
Chemical Substances	Isoenzymes ; Lactic Acid (33X04XA5AT) ; Pyruvic Acid (8558G7RUTR) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; lactate dehydrogenase 1 (EC 1.1.1.27.-)
Language	English
Publishing date	2020-05-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-2577-y
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Article ; Online: Proposed cytotoxic mechanisms of the saffron carotenoids crocin and crocetin on cancer cell lines.

Kim, Se Hyeuk / Lee, Jung Min / Kim, Sun Chang / Park, Chan Bae / Lee, Pyung Cheon

Biochemistry and cell biology = Biochimie et biologie cellulaire

2014 Volume 92, Issue 2, Page(s) 105–111

Abstract: We investigated the cytotoxic activities of crocin and crocetin, 2 major carotenoids isolated from the stigma of Crocus sativus (saffron), on 5 human cancer cell lines and proposed their possible anticancer mechanisms. Crocetin, a glycosylated carotenoid, ...

Abstract	We investigated the cytotoxic activities of crocin and crocetin, 2 major carotenoids isolated from the stigma of Crocus sativus (saffron), on 5 human cancer cell lines and proposed their possible anticancer mechanisms. Crocetin, a glycosylated carotenoid, showed approximately 5- to 18-fold higher cytotoxicity than crocin, a carboxylic carotenoid (IC50 of 0.16-0.61 mmol/L for crocetin vs. 2.0-5.5 mmol/L for crocin). This suggests that structural differences account for the different efficacies between them. Fluorescence-activated cell sorting (FACS) analysis showed that crocetin induced a significant level of cellular reactive oxygen species (ROS) in HeLa cells, whereas crocin did not. This ROS induction supported the cytotoxicity of crocetin, but not of crocin. A significant activation of nuclear factor erythroid 2-related factor 2 (Nrf2) was observed in both HeLa cells treated with crocin and crocetin: a 3.0-fold increase by 1 mmol/L crocetin and a 1.6-fold increase by 0.8 mmol/L crocin compared to the control. Furthermore, both crocetin and crocin reduced the protein expression of lactate dehydrogenase A (LDHA), one of the targets for chemoprevention in cancer cells, by 34.2% and 10.5%, respectively, compared to the control in HeLa cells. These findings suggest that crocetin and crocin have different mechanisms for their observed cytotoxicity in cancer cell lines.
MeSH term(s)	Carotenoids/pharmacology ; Cell Line, Tumor ; Crocus/chemistry ; Cytotoxins/pharmacology ; Female ; Humans ; Isoenzymes/metabolism ; L-Lactate Dehydrogenase/metabolism ; Lactate Dehydrogenase 5 ; NF-E2-Related Factor 2/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Cytotoxins ; Isoenzymes ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Reactive Oxygen Species ; trans-sodium crocetinate ; Carotenoids (36-88-4) ; crocin (877GWI46C2) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Lactate Dehydrogenase 5 (EC 1.1.1.27.-)
Language	English
Publishing date	2014-01-29
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	54104-7
ISSN	1208-6002 ; 0829-8211
ISSN (online)	1208-6002
ISSN	0829-8211
DOI	10.1139/bcb-2013-0091
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