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  1. Article ; Online: Healthy versus Unhealthy Adipose Tissue Expansion: the Role of Exercise.

    Meister, Benjamin M / Hong, Soon-Gook / Shin, Junchul / Rath, Meghan / Sayoc, Jacqueline / Park, Joon-Young

    Journal of obesity & metabolic syndrome

    2022  Volume 31, Issue 1, Page(s) 37–50

    Abstract: Although the hallmark of obesity is the expansion of adipose tissue, not all adipose tissue expansion is the same. Expansion of healthy adipose tissue is accompanied by adequate capillary angiogenesis and mitochondria-centered metabolic integrity, ... ...

    Abstract Although the hallmark of obesity is the expansion of adipose tissue, not all adipose tissue expansion is the same. Expansion of healthy adipose tissue is accompanied by adequate capillary angiogenesis and mitochondria-centered metabolic integrity, whereas expansion of unhealthy adipose tissue is associated with capillary and mitochondrial derangement, resulting in deposition of immune cells (M1-stage macrophages) and excess production of pro-inflammatory cytokines. Accumulation of these dysfunctional adipose tissues has been linked to the development of obesity comorbidities, such as type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease, which are leading causes of human mortality and morbidity in modern society. Mechanistically, vascular rarefaction and mitochondrial incompetency (for example, low mitochondrial content, fragmented mitochondria, defective mitochondrial respiratory function, and excess production of mitochondrial reactive oxygen species) are frequently observed in adipose tissue of obese patients. Recent studies have demonstrated that exercise is a potent behavioral intervention for preventing and reducing obesity and other metabolic diseases. However, our understanding of potential cellular mechanisms of exercise, which promote healthy adipose tissue expansion, is at the beginning stage. In this review, we hypothesize that exercise can induce unique physiological stimuli that can alter angiogenesis and mitochondrial remodeling in adipose tissues and ultimately promote the development and progression of healthy adipogenesis. We summarize recent reports on how regular exercise can impose differential processes that lead to the formation of either healthy or unhealthy adipose tissue and discuss key knowledge gaps that warrant future research.
    Language English
    Publishing date 2022-03-12
    Publishing country Korea (South)
    Document type Journal Article ; Review
    ZDB-ID 3021984-X
    ISSN 2508-7576 ; 2508-6235
    ISSN (online) 2508-7576
    ISSN 2508-6235
    DOI 10.7570/jomes21096
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mitochondrial and Metabolic Adaptations to Exercise-Induced Fluid Shear Stress in Endothelial Cells.

    Hong, Soon-Gook / Shin, Junchul / Aldokhayyil, Maitha / Brown, Michael David / Park, Joon-Young

    Exercise and sport sciences reviews

    2022  Volume 50, Issue 3, Page(s) 145–155

    Abstract: Recent studies have greatly advanced our understanding of the central role of mitochondria on endothelial function. Here, we propose a hypothesis that unidirectional laminar (pulsatile) flow and disturbed laminar (oscillatory) flow may differentially ... ...

    Abstract Recent studies have greatly advanced our understanding of the central role of mitochondria on endothelial function. Here, we propose a hypothesis that unidirectional laminar (pulsatile) flow and disturbed laminar (oscillatory) flow may differentially modulate mitochondrial phenotypes in the context of their bioenergetic, signaling, and biosynthetic functions, providing novel insights into subcellular mechanisms underlying how exercise benefits the improvement of vascular health.
    MeSH term(s) Cells, Cultured ; Endothelial Cells ; Endothelium, Vascular ; Humans ; Mitochondria ; Stress, Mechanical
    Language English
    Publishing date 2022-02-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187040-3
    ISSN 1538-3008 ; 0091-6331
    ISSN (online) 1538-3008
    ISSN 0091-6331
    DOI 10.1249/JES.0000000000000289
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Polarized Mechanosensitive Signaling Domains Protect Arterial Endothelial Cells Against Inflammation.

    Hong, Soon-Gook / Ashby, Julianne W / Kennelly, John P / Wu, Meigan / Chattopadhyay, Eesha / Foreman, Rob / Tontonoz, Peter / Turowski, Patric / Gallagher-Jones, Marcus / Mack, Julia J

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Endothelial cells (ECs) in the descending aorta are exposed to high laminar shear stress, which supports an anti-inflammatory phenotype that protects them from atherosclerosis. High laminar shear stress also supports flow-aligned cell elongation and ... ...

    Abstract Endothelial cells (ECs) in the descending aorta are exposed to high laminar shear stress, which supports an anti-inflammatory phenotype that protects them from atherosclerosis. High laminar shear stress also supports flow-aligned cell elongation and front-rear polarity, but whether this is required for athero-protective signaling is unclear. Here, we show that Caveolin-1-rich microdomains become polarized at the downstream end of ECs exposed to continuous high laminar flow. These microdomains are characterized by higher membrane rigidity, filamentous actin (F-actin) and lipid accumulation. Transient receptor potential vanilloid-type 4 (Trpv4) ion channels, while ubiquitously expressed, mediate localized Ca
    Language English
    Publishing date 2023-05-26
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.26.542500
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Effects of 12-Week Resistance Exercise on Electroencephalogram Patterns and Cognitive Function in the Elderly With Mild Cognitive Impairment: A Randomized Controlled Trial.

    Hong, Soon-Gook / Kim, June-Hong / Jun, Tae-Won

    Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine

    2017  Volume 28, Issue 6, Page(s) 500–508

    Abstract: Objective: To investigate the effects of a 12-week resistance exercise program with an elastic band on electroencephalogram (EEG) patterns and cognitive function in elderly patients with mild cognitive impairment (MCI).: Design: Randomized controlled ...

    Abstract Objective: To investigate the effects of a 12-week resistance exercise program with an elastic band on electroencephalogram (EEG) patterns and cognitive function in elderly patients with mild cognitive impairment (MCI).
    Design: Randomized controlled trial.
    Setting: Community center.
    Participants: Twenty-two subjects with MCI and 25 healthy volunteer subjects were randomly assigned to 1 of 4 groups: subjects with MCI who undertook the exercise program (MCI-EX; n = 10), an MCI control group (MCI-Con; n = 12), a healthy volunteer exercise group (NG-EX; n = 12), and a healthy volunteer control group (NG-Con; n = 13).
    Intervention: The exercise group engaged in a 15-repetition maximum (15RM; 65% of 1RM) resistance exercise program for 12 weeks.
    Main outcome measures: Electroencephalograms, neuropsychological tests, and Senior Fitness Test.
    Results: The 12-week 15RM (65% of 1RM) resistance exercise program significantly improved variables related to the physical fitness of the elderly subjects. Furthermore, for the EEG test, the MCI and NG groups showed significant differences at baseline in relative beta waves on electrodes Fp1 (P < 0.05) and F3 (P < 0.05), as well as in relative beta2 waves on F3 (P < 0.05). In addition, after the 12-week exercise intervention, differences in a region that benefits from exercise were observed between (1) the MCI-EX group in the relative theta power on F3 (P < 0.05) and the relative alpha power on T3 (P < 0.05) and in (2) the NG-EX group in the relative theta power on P3 (P < 0.05) and P4 (P < 0.01). In addition, only the score of the digit span backward in the MCI-EX group changed significantly (P < 0.05).
    Conclusions: The 12-week resistance exercise with an elastic band had a positive effect on EEG patterns in elderly subjects with MCI, along with providing physical benefits and slight changes in cognitive function in MCI-EX group.
    Significance: A 15RM resistance exercise program can be an effective treatment for delaying cognitive decline and improving physical fitness.
    MeSH term(s) Aged ; Aged, 80 and over ; Cognition ; Cognitive Dysfunction/therapy ; Electroencephalography ; Exercise Test ; Exercise Therapy ; Female ; Humans ; Male ; Neuropsychological Tests ; Resistance Training
    Language English
    Publishing date 2017-09-08
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial
    ZDB-ID 1062530-6
    ISSN 1536-3724 ; 1050-642X
    ISSN (online) 1536-3724
    ISSN 1050-642X
    DOI 10.1097/JSM.0000000000000476
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Flow-induced endothelial mitochondrial remodeling mitigates mitochondrial reactive oxygen species production and promotes mitochondrial DNA integrity in a p53-dependent manner.

    Shin, Junchul / Hong, Soon-Gook / Choi, Soo Young / Rath, Meghan E / Saredy, Jason / Jovin, Daniel G / Sayoc, Jacqueline / Park, Hye-Sang / Eguchi, Satoru / Rizzo, Victor / Scalia, Rosario / Wang, Hong / Houser, Steven R / Park, Joon-Young

    Redox biology

    2022  Volume 50, Page(s) 102252

    Abstract: Tumor suppressor p53 plays a pivotal role in orchestrating mitochondrial remodeling by regulating their content, fusion/fission processes, and intracellular signaling molecules that are associated with mitophagy and apoptosis pathways. In order to ... ...

    Abstract Tumor suppressor p53 plays a pivotal role in orchestrating mitochondrial remodeling by regulating their content, fusion/fission processes, and intracellular signaling molecules that are associated with mitophagy and apoptosis pathways. In order to determine a molecular mechanism underlying flow-mediated mitochondrial remodeling in endothelial cells, we examined, herein, the role of p53 on mitochondrial adaptations to physiological flow and its relevance to vascular function using endothelial cell-specific p53 deficient mice. We observed no changes in aerobic capacity, basal blood pressure, or endothelial mitochondrial phenotypes in the endothelial p53 mull animals. However, after 7 weeks of voluntary wheel running exercise, blood pressure reduction and endothelial mitochondrial remodeling (biogenesis, elongation, and mtDNA replication) were substantially blunted in endothelial p53 null animals compared to the wild-type, subjected to angiotensin II-induced hypertension. In addition, endothelial mtDNA lesions were significantly reduced following voluntary running exercise in wild-type mice, but not in the endothelial p53 null mice. Moreover, in vitro studies demonstrated that unidirectional laminar flow exposure significantly increased key putative regulators for mitochondrial remodeling and reduced mitochondrial reactive oxygen species generation and mtDNA damage in a p53-dependent manner. Mechanistically, unidirectional laminar flow instigated translocalization of p53 into the mitochondrial matrix where it binds to mitochondrial transcription factor A, TFAM, resulting in improving mtDNA integrity. Taken together, our findings suggest that p53 plays an integral role in mitochondrial remodeling under physiological flow condition and the flow-induced p53-TFAM axis may be a novel molecular intersection for enhancing mitochondrial homeostasis in endothelial cells.
    MeSH term(s) Animals ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Endothelial Cells/metabolism ; Mice ; Motor Activity ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances DNA, Mitochondrial ; Reactive Oxygen Species ; Trp53 protein, mouse ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2022-01-29
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2022.102252
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Flow pattern-dependent mitochondrial dynamics regulates the metabolic profile and inflammatory state of endothelial cells.

    Hong, Soon-Gook / Shin, Junchul / Choi, Soo Young / Powers, Jeffery C / Meister, Benjamin M / Sayoc, Jacqueline / Son, Jun Seok / Tierney, Ryan / Recchia, Fabio A / Brown, Michael D / Yang, Xiaofeng / Park, Joon-Young

    JCI insight

    2022  Volume 7, Issue 18

    Abstract: Endothelial mitochondria play a pivotal role in maintaining endothelial cell (EC) homeostasis through constantly altering their size, shape, and intracellular localization. Studies show that the disruption of the basal mitochondrial network in EC, ... ...

    Abstract Endothelial mitochondria play a pivotal role in maintaining endothelial cell (EC) homeostasis through constantly altering their size, shape, and intracellular localization. Studies show that the disruption of the basal mitochondrial network in EC, forming excess fragmented mitochondria, implicates cardiovascular disease. However, cellular consequences underlying the morphological changes in the endothelial mitochondria under distinctively different, but physiologically occurring, flow patterns (i.e., unidirectional flow [UF] versus disturbed flow [DF]) are largely unknown. The purpose of this study was to investigate the effect of different flow patterns on mitochondrial morphology and its implications in EC phenotypes. We show that mitochondrial fragmentation is increased at DF-exposed vessel regions, where elongated mitochondria are predominant in the endothelium of UF-exposed regions. DF increased dynamin-related protein 1 (Drp1), mitochondrial reactive oxygen species (mtROS), hypoxia-inducible factor 1, glycolysis, and EC activation. Inhibition of Drp1 significantly attenuated these phenotypes. Carotid artery ligation and microfluidics experiments further validate that the significant induction of mitochondrial fragmentation was associated with EC activation in a Drp1-dependent manner. Contrarily, UF in vitro or voluntary exercise in vivo significantly decreased mitochondrial fragmentation and enhanced fatty acid uptake and OXPHOS. Our data suggest that flow patterns profoundly change mitochondrial fusion/fission events, and this change contributes to the determination of proinflammatory and metabolic states of ECs.
    MeSH term(s) Dynamins ; Endothelial Cells/metabolism ; Fatty Acids/metabolism ; Hypoxia-Inducible Factor 1/metabolism ; Metabolome ; Mitochondrial Dynamics ; Reactive Oxygen Species/metabolism
    Chemical Substances Fatty Acids ; Hypoxia-Inducible Factor 1 ; Reactive Oxygen Species ; Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2022-09-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.159286
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Exercise training ameliorates cerebrovascular dysfunction in a murine model of Alzheimer's disease: role of the P2Y2 receptor and endoplasmic reticulum stress.

    Hong, Junyoung / Hong, Soon-Gook / Lee, Jonghae / Park, Joon-Young / Eriksen, Jason L / Rooney, Bridgette V / Park, Yoonjung

    American journal of physiology. Heart and circulatory physiology

    2020  Volume 318, Issue 6, Page(s) H1559–H1569

    Abstract: Cerebrovascular dysfunction is a critical risk factor for the pathogenesis of Alzheimer's disease (AD). The purinergic P2Y2 receptor and endoplasmic reticulum (ER) stress are tightly associated with vascular dysfunction and the pathogenesis of AD. ... ...

    Abstract Cerebrovascular dysfunction is a critical risk factor for the pathogenesis of Alzheimer's disease (AD). The purinergic P2Y2 receptor and endoplasmic reticulum (ER) stress are tightly associated with vascular dysfunction and the pathogenesis of AD. However, the protective effects of exercise training on P2Y2 receptor- and ER stress-associated cerebrovascular dysfunction in AD are mostly unknown. Control (C57BL/6, CON) and AD (APP/PS1dE9, AD) mice underwent treadmill exercise training (EX). 2-MeS-ATP-induced dose-dependent vasoreactivity was determined by using a pressurized posterior cerebral artery (PCA) from 10-12-mo-old mice. Human brain microvascular endothelial cells (HBMECs) were exposed to laminar shear stress (LSS) at 20 dyn/cm
    MeSH term(s) Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Animals ; Brain/metabolism ; Brain/physiopathology ; Cerebrovascular Circulation/physiology ; Disease Models, Animal ; Endoplasmic Reticulum Stress/physiology ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Mice ; Nitric Oxide Synthase Type III/metabolism ; Physical Conditioning, Animal/physiology ; Posterior Cerebral Artery/metabolism ; Posterior Cerebral Artery/physiopathology ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Purinergic P2Y2/metabolism
    Chemical Substances Receptors, Purinergic P2Y2 ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2020-05-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00129.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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