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Article ; Online: SARS-CoV-2-mediated evasion strategies for antiviral interferon pathways.

Oh, Soo-Jin / Shin, Ok Sarah

2022 Volume 60, Issue 3, Page(s) 290–299

Abstract: With global expansion of the COVID-19 pandemic and the emergence of new variants, extensive efforts have been made to develop highly effective antiviral drugs and vaccines against SARS-CoV-2. The interactions of coronaviruses with host antiviral ... ...

Abstract	With global expansion of the COVID-19 pandemic and the emergence of new variants, extensive efforts have been made to develop highly effective antiviral drugs and vaccines against SARS-CoV-2. The interactions of coronaviruses with host antiviral interferon pathways ultimately determine successful viral replication and SARS-CoV-2-induced pathogenesis. Innate immune receptors play an essential role in host defense against SARS-CoV-2 via the induction of IFN production and signaling. Here, we summarize the recent advances in innate immune sensing mechanisms of SARS-CoV-2 and various strategies by which SARS-CoV-2 antagonizes antiviral innate immune signaling pathways, with a particular focus on mechanisms utilized by multiple SARS-CoV-2 proteins to evade interferon induction and signaling in host cell. Understanding the underlying immune evasion mechanisms of SARS-CoV-2 is essential for the improvement of vaccines and therapeutic strategies.
MeSH term(s)	Antiviral Restriction Factors/immunology ; COVID-19/immunology ; COVID-19/virology ; Humans ; Immune Evasion ; Immunity, Innate ; Interferons/immunology ; Pandemics ; SARS-CoV-2
Chemical Substances	Antiviral Restriction Factors ; Interferons (9008-11-1)
Language	English
Publishing date	2022-02-05
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	2012399-1
ISSN	1976-3794 ; 1225-8873
ISSN (online)	1976-3794
ISSN	1225-8873
DOI	10.1007/s12275-022-1525-1
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Article ; Online: Role of Autophagy in the Pathogenesis of Diabetes and Therapeutic Potential of Autophagy Modulators in the Treatment of Diabetes and Metabolic Syndrome.

Oh, Soo-Jin / Lee, Myung-Shik

Journal of Korean medical science

2022 Volume 37, Issue 37, Page(s) e276

Abstract: Autophagy is critically involved in the maintenance of intracellular nutrient homeostasis and organelle function. Dysregulated autophagy is likely to play a role in the development of metabolic disorders and diabetes because autophagy is critical in the ... ...

Abstract	Autophagy is critically involved in the maintenance of intracellular nutrient homeostasis and organelle function. Dysregulated autophagy is likely to play a role in the development of metabolic disorders and diabetes because autophagy is critical in the rejuvenation of dysfunctional or stressed endoplasmic reticulum and mitochondria that play a crucial role in the development of diabetes. Indeed, systemic autophagy insufficiency led to the increased tissue lipid content, aggravated metabolic and finally more severe diabetes when metabolic stress was imposed, suggesting that autophagy insufficiency of dysfunction of lysosome, an effector organelle of autophagy, due to aging, genetic predisposition or environmental factors could be an underlying cause of diabetes. Conversely, autophagy enhancer could improve metabolic profile of obese mice by reducing tissue lipid content and ameliorating metabolic inflammation. Furthermore, clearance of human islet amyloid polypeptide (hIAPP) oligomer and amyloid that accumulate in pancreatic islets of > 90% of diabetes patients was also dependent on autophagy. Consistently, autophagy enhancer could improve glucose profile and β-cell function of transgenic mice expressing amyloidogenic hIAPP in pancreatic β-cells, which was accompanied by reduced accumulation of hIAPP oligomer or amyloid, ameliorated β-cell apoptosis and increased β-cell mass. These results suggest that autophagy enhancer could be a novel therapeutic modality against diabetes associated with lipid overload and human diabetes characterized by islet amyloid accumulation.
MeSH term(s)	Amyloid/genetics ; Amyloid/metabolism ; Animals ; Autophagy/physiology ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/pathology ; Diabetes Mellitus, Type 2/pathology ; Glucose/metabolism ; Humans ; Insulin-Secreting Cells/metabolism ; Islet Amyloid Polypeptide/chemistry ; Islet Amyloid Polypeptide/genetics ; Islet Amyloid Polypeptide/metabolism ; Islets of Langerhans/metabolism ; Islets of Langerhans/pathology ; Lipids ; Metabolic Syndrome/complications ; Mice ; Mice, Transgenic
Chemical Substances	Amyloid ; Islet Amyloid Polypeptide ; Lipids ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-09-26
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	639262-3
ISSN	1598-6357 ; 1011-8934
ISSN (online)	1598-6357
ISSN	1011-8934
DOI	10.3346/jkms.2022.37.e276
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Article: Lysosomal Ca

Oh, Soo-Jin / Hwang, Yeseong / Hur, Kyu Yeon / Lee, Myung-Shik

Cell death discovery

2023 Volume 9, Issue 1, Page(s) 100

Abstract: While the mechanism of lipotoxicity by palmitic acid (PA), an effector of metabolic stress in vitro and in vivo, has been extensively investigated, molecular details of lipotoxicity are still not fully characterized. Since recent studies reported that PA ...

Abstract	While the mechanism of lipotoxicity by palmitic acid (PA), an effector of metabolic stress in vitro and in vivo, has been extensively investigated, molecular details of lipotoxicity are still not fully characterized. Since recent studies reported that PA can exert lysosomal stress in addition to well-known ER and mitochondrial stress, we studied the role of lysosomal events in lipotoxicity by PA, focusing on lysosomal Ca
Language	English
Publishing date	2023-03-21
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-023-01379-0
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Article ; Online: Is it appropriate to use external loads during side-lying hip abduction exercise for weakened gluteus medius?

Nam, Soo-Jin / Oh, Duck-Won

Journal of back and musculoskeletal rehabilitation

2021 Volume 34, Issue 6, Page(s) 1057–1062

Abstract: Background: Side-lying hip abduction exercise could be beneficial to improve the neuromuscular control of the hip abductor; however, there has been limited information available to determine the exercise load during the exercise.: Objective: This ... ...

Abstract	Background: Side-lying hip abduction exercise could be beneficial to improve the neuromuscular control of the hip abductor; however, there has been limited information available to determine the exercise load during the exercise. Objective: This study aimed to demonstrate the effects of using external loads on the hip abductor muscles during side-lying hip abduction exercises in females with gluteus medius (GM) weakness. Methods: This study enrolled 24 females with weakness in the GM. Electromyographic (EMG) data of the quadratus lumborum (QL) and GM muscles were recorded during the exercise under three load conditions: no-load, external load-1 (3% of body weight), and external load-2 (5% of body weight). Results: During the exercise, the EMG activities of the QL were significantly different under all three conditions (p< 0.05), with greater activity observed in the external load-2 condition (92.05 ± 65.93% maximal voluntary isometric contraction [MVIC]) as compared to the others, and in the external load-1 condition (82.47 ± 57.36% MVIC) as compared to the no-load condition (48.94 ± 45.09% MVIC). Furthermore, the GM/QL ratios showed significant differences between no-load (1.78 ± 1.47) and external load-1 conditions (0.93 ± 0.60), and between no-load and external load-2 (0.85 ± 0.45) conditions (p< 0.05). Conclusion: These findings suggest that greater load could be a factor to increase the QL activity during the exercise in females with weakened GM.
MeSH term(s)	Buttocks ; Electromyography ; Female ; Hip Joint ; Humans ; Muscle, Skeletal ; Thigh
Language	English
Publishing date	2021-03-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1184721-9
ISSN	1878-6324 ; 1053-8127
ISSN (online)	1878-6324
ISSN	1053-8127
DOI	10.3233/BMR-200108
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Article ; Online: Theophylline Attenuates BLM-Induced Pulmonary Fibrosis by Inhibiting Th17 Differentiation.

Park, Soo-Jin / Hahn, Hwa-Jeong / Oh, Sei-Ryang / Lee, Hyun-Jun

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a chronic and refractory interstitial lung disease. Although there are two approved drugs for IPF, they were not able to completely cure the disease. Therefore, the development of new drugs is required for the effective treatment of IPF. In this study, we investigated the effect of theophylline, which has long been used for the treatment of asthma, on pulmonary fibrosis. The administration of theophylline attenuated the fibrotic changes of lung tissues and improved mechanical pulmonary functions in bleomycin (BLM)-induced pulmonary fibrosis. Theophylline treatment suppressed IL-17 production through inhibiting cytokines controlling Th17 differentiation; TGF-β, IL-6, IL-1β, and IL-23. The inhibition of IL-6 and IL-1β by theophylline is mediated by suppressing BLM-induced ROS production and NF-κB activation in epithelial cells. We further demonstrated that theophylline inhibited TGF-β-induced epithelial-to-mesenchymal transition in epithelial cells through suppressing the phosphorylation of Smad2/3 and AKT. The inhibitory effects of theophylline on the phosphorylation of Smad2/3 and AKT were recapitulated in BLM-treated lung tissues. Taken together, these results demonstrated that theophylline prevents pulmonary fibrosis by inhibiting Th17 differentiation and TGF-β signaling.
MeSH term(s)	Animals ; Mice ; Bleomycin/toxicity ; Theophylline/pharmacology ; Interleukin-6/pharmacology ; Proto-Oncogene Proteins c-akt ; Lung ; Cell Differentiation ; Transforming Growth Factor beta/pharmacology ; Idiopathic Pulmonary Fibrosis/chemically induced ; Idiopathic Pulmonary Fibrosis/drug therapy ; Mice, Inbred C57BL
Chemical Substances	Bleomycin (11056-06-7) ; Theophylline (C137DTR5RG) ; Interleukin-6 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Transforming Growth Factor beta
Language	English
Publishing date	2023-01-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24021019
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: SARS-CoV-2-mediated evasion strategies for antiviral interferon pathways

Oh, Soo-Jin / Shin, Ok Sarah

journal of microbiology. 2022 Mar., v. 60, no. 3

2022

Abstract	With global expansion of the COVID-19 pandemic and the emergence of new variants, extensive efforts have been made to develop highly effective antiviral drugs and vaccines against SARS-CoV-2. The interactions of coronaviruses with host antiviral interferon pathways ultimately determine successful viral replication and SARS-CoV-2-induced pathogenesis. Innate immune receptors play an essential role in host defense against SARS-CoV-2 via the induction of IFN production and signaling. Here, we summarize the recent advances in innate immune sensing mechanisms of SARS-CoV-2 and various strategies by which SARS-CoV-2 antagonizes antiviral innate immune signaling pathways, with a particular focus on mechanisms utilized by multiple SARS-CoV-2 proteins to evade interferon induction and signaling in host cell. Understanding the underlying immune evasion mechanisms of SARS-CoV-2 is essential for the improvement of vaccines and therapeutic strategies.
Keywords	COVID-19 infection ; Severe acute respiratory syndrome coronavirus 2 ; immune evasion ; interferons ; pathogenesis ; therapeutics ; virus replication
Language	English
Dates of publication	2022-03
Size	p. 290-299.
Publishing place	The Microbiological Society of Korea
Document type	Article
Note	Review
ZDB-ID	2012399-1
ISSN	1225-8873
ISSN	1225-8873
DOI	10.1007/s12275-022-1525-1
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Varicella zoster virus glycoprotein E facilitates PINK1/Parkin-mediated mitophagy to evade STING and MAVS-mediated antiviral innate immunity.

Oh, Soo-Jin / Yu, Je-Wook / Ahn, Jin-Hyun / Choi, Seok Tae / Park, Hosun / Yun, Jeanho / Shin, Ok Sarah

Cell death & disease

2024 Volume 15, Issue 1, Page(s) 16

Abstract: Viruses have evolved to control mitochondrial quality and content to facilitate viral replication. Mitophagy is a selective autophagy, in which the damaged or unnecessary mitochondria are removed, and thus considered an essential mechanism for ... ...

Abstract	Viruses have evolved to control mitochondrial quality and content to facilitate viral replication. Mitophagy is a selective autophagy, in which the damaged or unnecessary mitochondria are removed, and thus considered an essential mechanism for mitochondrial quality control. Although mitophagy manipulation by several RNA viruses has recently been reported, the effect of mitophagy regulation by varicella zoster virus (VZV) remains to be fully determined. In this study, we showed that dynamin-related protein-1 (DRP1)-mediated mitochondrial fission and subsequent PINK1/Parkin-dependent mitophagy were triggered during VZV infection, facilitating VZV replication. In addition, VZV glycoprotein E (gE) promoted PINK1/Parkin-mediated mitophagy by interacting with LC3 and upregulating mitochondrial reactive oxygen species. Importantly, VZV gE inhibited MAVS oligomerization and STING translocation to disrupt MAVS- and STING-mediated interferon (IFN) responses, and PINK1/Parkin-mediated mitophagy was required for VZV gE-mediated inhibition of IFN production. Similarly, carbonyl cyanide m-chlorophenyl hydrazone (CCCP)-mediated mitophagy induction led to increased VZV replication but attenuated IFN production in a three-dimensional human skin organ culture model. Our results provide new insights into the immune evasion mechanism of VZV gE via PINK1/Parkin-dependent mitophagy.
MeSH term(s)	Humans ; Mitophagy ; Immunity, Innate ; Carbonyl Cyanide m-Chlorophenyl Hydrazone ; Ubiquitin-Protein Ligases ; Antiviral Agents ; Protein Kinases
Chemical Substances	glycoprotein E, varicella-zoster virus ; Carbonyl Cyanide m-Chlorophenyl Hydrazone (555-60-2) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Antiviral Agents ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2024-01-06
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/s41419-023-06400-z
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Article ; Online: Potentiality to natural immunization inducement against VHS in olive flounder by live VHSV immersion vaccination at temperature controlled culture condition.

Kim, Soo-Jin / Oh, Myung-Joo

Virus research

2020 Volume 288, Page(s) 198140

Abstract: Viral hemorrhagic septicemia virus (VHSV) is the etiological agent of viral hemorrhagic septicemia (VHS), one of the most severe viral diseases affecting cultured olive flounder (Paralichthys olivaceus) in Far East Asia. VHS occurs during the winter or ... ...

Abstract	Viral hemorrhagic septicemia virus (VHSV) is the etiological agent of viral hemorrhagic septicemia (VHS), one of the most severe viral diseases affecting cultured olive flounder (Paralichthys olivaceus) in Far East Asia. VHS occurs during the winter or spring season when the water temperature is low (9-15 °C). In our previous study found that VHSV infection had controlled by using water temperature (above 17 °C). By using water temperature, we demonstrated optimal live VHSV immersion vaccine treatment concentration, also live VHSV immersion vaccine treatment method. We confirmed that the effective VHSV immersion treatment was 10
MeSH term(s)	Animals ; Aquaculture/methods ; Fish Diseases/prevention & control ; Fish Diseases/virology ; Flounder/immunology ; Flounder/virology ; Hemorrhagic Septicemia, Viral/immunology ; Hemorrhagic Septicemia, Viral/prevention & control ; Immersion ; Immunity, Innate ; Temperature ; Vaccination/methods ; Vaccination/veterinary ; Vaccines, Attenuated/pharmacology ; Viral Vaccines/pharmacology
Chemical Substances	Vaccines, Attenuated ; Viral Vaccines
Language	English
Publishing date	2020-08-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605780-9
ISSN	1872-7492 ; 0168-1702
ISSN (online)	1872-7492
ISSN	0168-1702
DOI	10.1016/j.virusres.2020.198140
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Article ; Online: Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Soo-Jin Oh / Kihyoun Park / Seong Keun Sonn / Goo Taeg Oh / Myung-Shik Lee

Experimental and Molecular Medicine, Vol 55, Iss 9, Pp 1922-

2023 Volume 1932

Abstract: Abstract Mitophagy is an excellent example of selective autophagy that eliminates damaged or dysfunctional mitochondria, and it is crucial for the maintenance of mitochondrial integrity and function. The critical roles of autophagy in pancreatic β-cell ... ...

Abstract	Abstract Mitophagy is an excellent example of selective autophagy that eliminates damaged or dysfunctional mitochondria, and it is crucial for the maintenance of mitochondrial integrity and function. The critical roles of autophagy in pancreatic β-cell structure and function have been clearly shown. Furthermore, morphological abnormalities and decreased function of mitochondria have been observed in autophagy-deficient β-cells, suggesting the importance of β-cell mitophagy. However, the role of authentic mitophagy in β-cell function has not been clearly demonstrated, as mice with pancreatic β-cell-specific disruption of Parkin, one of the most important players in mitophagy, did not exhibit apparent abnormalities in β-cell function or glucose homeostasis. Instead, the role of mitophagy in pancreatic β-cells has been investigated using β-cell-specific Tfeb-knockout mice (Tfeb Δβ-cell mice); Tfeb is a master regulator of lysosomal biogenesis or autophagy gene expression and participates in mitophagy. Tfeb Δβ-cell mice were unable to adaptively increase mitophagy or mitochondrial complex activity in response to high-fat diet (HFD)-induced metabolic stress. Consequently, Tfeb Δβ-cell mice exhibited impaired β-cell responses and further exacerbated metabolic deterioration after HFD feeding. TFEB was activated by mitochondrial or metabolic stress-induced lysosomal Ca2+ release, which led to calcineurin activation and mitophagy. After lysosomal Ca2+ release, depleted lysosomal Ca2+ stores were replenished by ER Ca2+ through ER→lysosomal Ca2+ refilling, which supplemented the low lysosomal Ca2+ capacity. The importance of mitophagy in β-cell function was also demonstrated in mice that developed β-cell dysfunction and glucose intolerance after treatment with a calcineurin inhibitor that hampered TFEB activation and mitophagy.
Keywords	Medicine ; R ; Biochemistry ; QD415-436
Subject code	572 ; 570
Language	English
Publishing date	2023-09-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The role of astrocytic γ-aminobutyric acid in the action of inhalational anesthetics.

Won, Dongwook / Lee, Elliot H / Chang, Jee-Eun / Nam, Min-Ho / Park, Ki Duk / Oh, Soo-Jin / Hwang, Jin-Young

European journal of pharmacology

2024 Volume 970, Page(s) 176494

Abstract: Background: Inhalational anesthetics target the inhibitory extrasynaptic γ-aminobutyric acid type A (GABA: Methods: Gene knockout of monoamine oxidase B (MAOB) was used to reduce astrocytic GABA levels in mice. The hypnotic and immobilizing effects ... ...

Abstract	Background: Inhalational anesthetics target the inhibitory extrasynaptic γ-aminobutyric acid type A (GABA Methods: Gene knockout of monoamine oxidase B (MAOB) was used to reduce astrocytic GABA levels in mice. The hypnotic and immobilizing effects of isoflurane, sevoflurane, and desflurane were assessed by evaluating the loss of righting reflex (LORR) and tail-pinch withdrawal response (LTWR) in MAOB knockout and wild-type mice. Minimum alveolar concentration (MAC) for LORR, time to LORR, MAC for LTWR and time to LTWR of isoflurane, sevoflurane, and desflurane were assessed. Results: Time to LORR and time to LTWR with isoflurane were significantly longer in MAOB knockout mice than in wild-type mice (P < 0.001 and P = 0.032, respectively). Time to LORR with 0.8 MAC of sevoflurane was significantly longer in MAOB knockout mice than in wild-type mice (P < 0.001), but not with 1.0 MAC of sevoflurane (P=0.217). MAC for LTWR was significantly higher in MAOB knockout mice exposed to sevoflurane (P < 0.001). With desflurane, MAOB knockout mice had a significantly higher MAC for LORR (P = 0.003) and higher MAC for LTWR (P < 0.001) than wild-type mice. Conclusions: MAOB knockout mice showed reduced sensitivity to the hypnotic and immobilizing effects of isoflurane, sevoflurane, and desflurane. Behavioral tests revealed that the hypnotic and immobilizing effects of inhalational anesthetics would be mediated by astrocytic GABA.
MeSH term(s)	Mice ; Animals ; Isoflurane/pharmacology ; Sevoflurane/pharmacology ; Desflurane/pharmacology ; Anesthetics, Inhalation/pharmacology ; gamma-Aminobutyric Acid ; Hypnotics and Sedatives ; Mice, Knockout ; Receptors, GABA-A ; Methyl Ethers/pharmacology
Chemical Substances	Isoflurane (CYS9AKD70P) ; Sevoflurane (38LVP0K73A) ; Desflurane (CRS35BZ94Q) ; Anesthetics, Inhalation ; gamma-Aminobutyric Acid (56-12-2) ; Hypnotics and Sedatives ; Receptors, GABA-A ; Methyl Ethers
Language	English
Publishing date	2024-03-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2024.176494
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