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Article ; Online: The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model.

Boylan, Brendan T / Hwang, Mihyun / Bergmann, Cornelia C

2023 Volume 15, Issue 12

Abstract: Recognition of viruses invading the central nervous system (CNS) by pattern recognition receptors (PRRs) is crucial to elicit early innate responses that stem dissemination. These innate responses comprise both type I interferon (IFN-I)-mediated defenses ...

Abstract	Recognition of viruses invading the central nervous system (CNS) by pattern recognition receptors (PRRs) is crucial to elicit early innate responses that stem dissemination. These innate responses comprise both type I interferon (IFN-I)-mediated defenses as well as signals recruiting leukocytes to control the infection. Focusing on insights from the neurotropic mouse CoV model, this review discusses how early IFN-I, fibroblast, and myeloid signals can influence protective anti-viral adaptive responses. Emphasis is placed on three main areas: the importance of coordinating the distinct capacities of resident CNS cells to induce and respond to IFN-I, the effects of select IFN-stimulated genes (ISGs) on host immune responses versus viral control, and the contribution of fibroblast activation and myeloid cells in aiding the access of T cells to the parenchyma. By unraveling how the dysregulation of early innate components influences adaptive immunity and viral control, this review illustrates the combined effort of resident CNS cells to achieve viral control.
MeSH term(s)	Mice ; Animals ; Coronavirus ; Encephalomyelitis ; Central Nervous System ; Interferon Type I ; Coronavirus Infections ; Immunity, Innate
Chemical Substances	Interferon Type I
Language	English
Publishing date	2023-12-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v15122400
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Neuronal Ablation of Alpha/Beta Interferon (IFN-α/β) Signaling Exacerbates Central Nervous System Viral Dissemination and Impairs IFN-γ Responsiveness in Microglia/Macrophages.

Hwang, Mihyun / Bergmann, Cornelia C

Journal of virology

2020 Volume 94, Issue 20

Abstract: Alpha/beta interferon (IFN-α/β) signaling through the IFN-α/β receptor (IFNAR) is essential to limit virus dissemination throughout the central nervous system (CNS) following many neurotropic virus infections. However, the distinct expression patterns of ...

Abstract	Alpha/beta interferon (IFN-α/β) signaling through the IFN-α/β receptor (IFNAR) is essential to limit virus dissemination throughout the central nervous system (CNS) following many neurotropic virus infections. However, the distinct expression patterns of factors associated with the IFN-α/β pathway in different CNS resident cell populations implicate complex cooperative pathways in IFN-α/β induction and responsiveness. Here we show that mice devoid of IFNAR1 signaling in calcium/calmodulin-dependent protein kinase II alpha (CaMKIIα) expressing neurons (CaMKIIcre:IFNAR
MeSH term(s)	Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Central Nervous System/immunology ; Central Nervous System/virology ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Disease Models, Animal ; Encephalomyelitis/immunology ; Encephalomyelitis/virology ; Interferon Type I/metabolism ; Interferon-gamma/metabolism ; Macrophages/metabolism ; Macrophages/virology ; Mice ; Mice, Mutant Strains ; Microglia/metabolism ; Microglia/virology ; Murine hepatitis virus/physiology ; Neurons/metabolism ; Neurons/virology ; Neutrophil Infiltration ; Receptor, Interferon alpha-beta/deficiency ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/metabolism ; Signal Transduction ; Virus Replication
Chemical Substances	Ifnar1 protein, mouse ; Interferon Type I ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferon-gamma (82115-62-6) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Camk2a protein, mouse (EC 2.7.11.17)
Keywords	covid19
Language	English
Publishing date	2020-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00422-20
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Article ; Online: Alpha/Beta Interferon (IFN-α/β) Signaling in Astrocytes Mediates Protection against Viral Encephalomyelitis and Regulates IFN-γ-Dependent Responses.

Hwang, Mihyun / Bergmann, Cornelia C

Journal of virology

2018 Volume 92, Issue 10

Abstract: The contribution of distinct central nervous system (CNS) resident cells to protective alpha/beta interferon (IFN-α/β) function following viral infections is poorly understood. Based on numerous immune regulatory functions of astrocytes, we evaluated the ...

Abstract	The contribution of distinct central nervous system (CNS) resident cells to protective alpha/beta interferon (IFN-α/β) function following viral infections is poorly understood. Based on numerous immune regulatory functions of astrocytes, we evaluated the contribution of astrocyte IFN-α/β signaling toward protection against the nonlethal glia- and neuronotropic mouse hepatitis virus (MHV) strain A59. Analysis of gene expression associated with IFN-α/β function, e.g., pattern recognition receptors (PRRs) and interferon-stimulated genes (ISGs), revealed lower basal mRNA levels in brain-derived astrocytes than in microglia. Although astrocytes poorly induced
MeSH term(s)	Animals ; Astrocytes/immunology ; Astrocytes/virology ; Central Nervous System/immunology ; Central Nervous System/virology ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Encephalomyelitis/immunology ; Encephalomyelitis/virology ; Interferon-alpha/immunology ; Interferon-beta/immunology ; Interferon-gamma/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Murine hepatitis virus/immunology ; Receptor, Interferon alpha-beta/genetics ; Signal Transduction/immunology
Chemical Substances	Interferon-alpha ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferon-beta (77238-31-4) ; Interferon-gamma (82115-62-6)
Keywords	covid19
Language	English
Publishing date	2018-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01901-17
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Article ; Online: Intercellular Communication Is Key for Protective IFNα/β Signaling During Viral Central Nervous System Infection.

Hwang, Mihyun / Bergmann, Cornelia C

Viral immunology

2018 Volume 32, Issue 1, Page(s) 1–6

Abstract: A variety of viruses can induce central nervous system (CNS) infections and neurological diseases, although the incidence is rare. Similar to peripheral infections, IFNα/β induction and signaling constitutes a first line of defense to limit virus ... ...

Abstract	A variety of viruses can induce central nervous system (CNS) infections and neurological diseases, although the incidence is rare. Similar to peripheral infections, IFNα/β induction and signaling constitutes a first line of defense to limit virus dissemination. However, CNS-resident cells differ widely in their repertoire and magnitude of both basal and inducible components in the IFNα/β pathway. While microglia as resident myeloid cells have been implicated as prominent sentinels of CNS invading pathogens or insults, astrocytes are emerging as key responders to many neurotropic RNA virus infections. Focusing on RNA viruses, this review discusses the role of astrocytes as IFNα/β inducers and responders and touches on the role of IFNα/β receptor signaling in regulating myeloid cell activation and IFNγ responsiveness. A summary picture emerges implicating IFNα/β not only as key in establishing the classical "antiviral" state, but also orchestrating cell mobility and IFNγ-mediated effector functions.
MeSH term(s)	Animals ; Astrocytes/virology ; Central Nervous System Viral Diseases/immunology ; Humans ; Interferon-alpha/immunology ; Interferon-beta/immunology ; Interferon-gamma/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia/virology ; RNA Viruses ; Signal Transduction
Chemical Substances	Interferon-alpha ; Interferon-beta (77238-31-4) ; Interferon-gamma (82115-62-6)
Keywords	covid19
Language	English
Publishing date	2018-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	639075-4
ISSN	1557-8976 ; 0882-8245
ISSN (online)	1557-8976
ISSN	0882-8245
DOI	10.1089/vim.2018.0101
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Zs.A 2227: Show issues

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Article: Neuronal Ablation of Alpha/Beta Interferon (IFN-α/ß) Signaling Exacerbates Central Nervous System Viral Dissemination and Impairs IFN-Î³ Responsiveness in Microglia/Macrophages

Hwang, Mihyun / Bergmann, Cornelia C

J. virol

Abstract: Alpha/beta interferon (IFN-α/ß) signaling through the IFN-α/ß receptor (IFNAR) is essential to limit virus dissemination throughout the central nervous system (CNS) following many neurotropic virus infections. However, the distinct expression patterns of ...

Abstract	Alpha/beta interferon (IFN-α/ß) signaling through the IFN-α/ß receptor (IFNAR) is essential to limit virus dissemination throughout the central nervous system (CNS) following many neurotropic virus infections. However, the distinct expression patterns of factors associated with the IFN-α/ß pathway in different CNS resident cell populations implicate complex cooperative pathways in IFN-α/ß induction and responsiveness. Here we show that mice devoid of IFNAR1 signaling in calcium/calmodulin-dependent protein kinase II alpha (CaMKIIα) expressing neurons (CaMKIIcre:IFNARfl/fl mice) infected with a mildly pathogenic neurotropic coronavirus (mouse hepatitis virus A59 strain [MHV-A59]) developed severe encephalomyelitis with hind-limb paralysis and succumbed within 7 days. Increased virus spread in CaMKIIcre:IFNARfl/fl mice compared to IFNARfl/fl mice affected neurons not only in the forebrain but also in the mid-hind brain and spinal cords but excluded the cerebellum. Infection was also increased in glia. The lack of viral control in CaMKIIcre:IFNARfl/fl relative to control mice coincided with sustained Cxcl1 and Ccl2 mRNAs but a decrease in mRNA levels of IFNα/ß pathway genes as well as Il6, Tnf, and Il1ß between days 4 and 6 postinfection (p.i.). T cell accumulation and IFN-Î³ production, an essential component of virus control, were not altered. However, IFN-Î³ responsiveness was impaired in microglia/macrophages irrespective of similar pSTAT1 nuclear translocation as in infected controls. The results reveal how perturbation of IFN-α/ß signaling in neurons can worsen disease course and disrupt complex interactions between the IFN-α/ß and IFN-Î³ pathways in achieving optimal antiviral responses.IMPORTANCE IFN-α/ß induction limits CNS viral spread by establishing an antiviral state, but also promotes blood brain barrier integrity, adaptive immunity, and activation of microglia/macrophages. However, the extent to which glial or neuronal signaling contributes to these diverse IFN-α/ß functions is poorly understood. Using a neurotropic mouse hepatitis virus encephalomyelitis model, this study demonstrated an essential role of IFN-α/ß receptor 1 (IFNAR1) specifically in neurons to control virus spread, regulate IFN-Î³ signaling, and prevent acute mortality. The results support the notion that effective neuronal IFNAR1 signaling compensates for their low basal expression of genes in the IFN-α/ß pathway compared to glia. The data further highlight the importance of tightly regulated communication between the IFN-α/ß and IFN-Î³ signaling pathways to optimize antiviral IFN-Î³ activity.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #840609
Database	COVID19

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Article ; Online: Trem2 deficiency impairs recovery and phagocytosis and dysregulates myeloid gene expression during virus-induced demyelination.

Hwang, Mihyun / Savarin, Carine / Kim, Jihye / Powers, Jennifer / Towne, Natasha / Oh, Hyunsuk / Bergmann, Cornelia C

Journal of neuroinflammation

2022 Volume 19, Issue 1, Page(s) 267

Abstract: Background: Triggering receptor expressed on myeloid cells 2 (Trem2) plays a protective role in neurodegenerative diseases. By contrast, Trem2 functions can exacerbate tissue damage during respiratory viral or liver infections. We, therefore, ... ...

Abstract	Background: Triggering receptor expressed on myeloid cells 2 (Trem2) plays a protective role in neurodegenerative diseases. By contrast, Trem2 functions can exacerbate tissue damage during respiratory viral or liver infections. We, therefore, investigated the role of Trem2 in a viral encephalomyelitis model associated with prominent Th1 mediated antiviral immunity leading to demyelination. Methods: Wild-type (WT) and Trem2 deficient (Trem2 Results: BMDM recruited to SCs in response to infection highly upregulated Trem2 mRNA compared to microglia coincident with viral control. Trem2 deficiency did not alter disease onset or severity, but impaired clinical recovery after onset of demyelination. Disease progression in Trem2 Conclusions: Trem2 deficiency during viral-induced demyelination dysregulates expression of other select genes regulating phagocytic pathways and lipid metabolism, with distinct effects on microglia and BMDM. The ultimate failure to remove damaged myelin is reminiscent of toxin or autoimmune cell-induced demyelination models and supports that Trem2 function is regulated by sensing tissue damage including a dysregulated lipid environment in very distinct inflammatory environments.
MeSH term(s)	Animals ; Mice ; Brain/metabolism ; Phagocytosis/genetics ; Microglia/metabolism ; Demyelinating Diseases/chemically induced ; Disease Progression ; Gene Expression ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism
Chemical Substances	Trem2 protein, mouse ; Membrane Glycoproteins ; Receptors, Immunologic
Language	English
Publishing date	2022-11-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-022-02629-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dynamics of Virus-Specific Memory B Cells and Plasmablasts following Viral Infection of the Central Nervous System.

Atkinson, Jeffrey R / Hwang, Mihyun / Reyes-Rodriguez, Angel / Bergmann, Cornelia C

Journal of virology

2019 Volume 93, Issue 2

Abstract: Humoral responses within the central nervous system (CNS) are common to many neurotropic viral infections, with antibody (Ab)-secreting cells (ASC) contributing to local protection. However, a role for virus-specific memory B cells (Bmem) within the CNS ... ...

Abstract	Humoral responses within the central nervous system (CNS) are common to many neurotropic viral infections, with antibody (Ab)-secreting cells (ASC) contributing to local protection. However, a role for virus-specific memory B cells (Bmem) within the CNS is poorly explored due to lack of robust phenotypic or functional identification in mice. This study takes advantage of the progeny of mice expressing tamoxifen-inducible Cre recombinase (Cre-ERT2) under the
MeSH term(s)	Animals ; Antibodies, Viral/metabolism ; B-Lymphocytes/immunology ; Central Nervous System/immunology ; Central Nervous System/virology ; Coronavirus/immunology ; Cytidine Deaminase/metabolism ; Female ; Germinal Center/immunology ; Male ; Mice ; Somatic Hypermutation, Immunoglobulin
Chemical Substances	Antibodies, Viral ; Cytidine Deaminase (EC 3.5.4.5)
Keywords	covid19
Language	English
Publishing date	2019-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00875-18
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Analysis of hypoxanthine and lactic acid levels in vitreous humor for the estimation of post-mortem interval (PMI) using LC-MS/MS.

Go, Ahra / Shim, Geunae / Park, Jiwon / Hwang, Jinwoo / Nam, Mihyun / Jeong, Hankyung / Chung, Heesun

Forensic science international

2019 Volume 299, Page(s) 135–141

Abstract: Hypoxanthine (Hx) is produced during terminal stages of purine catabolism in humans. The concentrations of Hx and l-lactic acid in vitreous humor highly correlate with post-mortem interval (PMI). In this study, we measured the concentrations of Hx and l- ... ...

Abstract	Hypoxanthine (Hx) is produced during terminal stages of purine catabolism in humans. The concentrations of Hx and l-lactic acid in vitreous humor highly correlate with post-mortem interval (PMI). In this study, we measured the concentrations of Hx and l-lactic acid in uncontrolled authentic vitreous humor from cadavers, and investigated the correlation between these molecules and PMI. A liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used for the quantitative analysis of Hx and l-lactic acid in vitreous humor. These concentrations were also corrected by four seasons such as spring, summer, autumn, and winter and temperatures on the day of death such as -10 to 5 °C, 6-15 °C, 16-25 °C, and 26-32 °C that may affect the biomarker concentrations. Vitreous humors were collected from cadavers with known time of death at the National Forensic Service (NFS), Republic of Korea. The correlation between the concentrations of Hx and l-lactic acid in vitreous humors and PMI was evaluated using 79 corpses (53 males and 26 females), with sampling time ranging from 13 to 103 h after death. The average daily ambient temperature at the time of death of each sample was investigated to calibrate the correlation with PMI. Following correction of the concentrations of Hx and l-lactic acid with temperature, the correlation of Hx and l-lactic acid with PMI increased from 0.53 to 0.59 for Hx and 0.38 to 0.42 for l-lactic acid. The highest correlation of Hx and l-lactic acid concentrations with PMI was observed in the winter season, with an R
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cadaver ; Child ; Chromatography, Liquid ; Female ; Forensic Pathology/methods ; Humans ; Hypoxanthine/metabolism ; Lactic Acid/metabolism ; Male ; Middle Aged ; Postmortem Changes ; Seasons ; Tandem Mass Spectrometry ; Temperature ; Vitreous Body/metabolism ; Young Adult
Chemical Substances	Hypoxanthine (2TN51YD919) ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2019-04-01
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	424042-x
ISSN	1872-6283 ; 0379-0738
ISSN (online)	1872-6283
ISSN	0379-0738
DOI	10.1016/j.forsciint.2019.03.024
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Article: Analysis of hypoxanthine and lactic acid levels in vitreous humor for the estimation of post-mortem interval (PMI) using LC–MS/MS

Go, Ahra / Chung, Heesun / Hwang, Jinwoo / Jeong, Hankyung / Nam, Mihyun / Park, Jiwon / Shim, Geunae

Forensic science international. 2019 June, v. 299

2019

Abstract	Hypoxanthine (Hx) is produced during terminal stages of purine catabolism in humans. The concentrations of Hx and l-lactic acid in vitreous humor highly correlate with post-mortem interval (PMI). In this study, we measured the concentrations of Hx and l-lactic acid in uncontrolled authentic vitreous humor from cadavers, and investigated the correlation between these molecules and PMI. A liquid chromatography–tandem mass spectrometry (LC–MS/MS) was used for the quantitative analysis of Hx and l-lactic acid in vitreous humor. These concentrations were also corrected by four seasons such as spring, summer, autumn, and winter and temperatures on the day of death such as −10 to 5 °C, 6–15 °C, 16–25 °C, and 26–32 °C that may affect the biomarker concentrations. Vitreous humors were collected from cadavers with known time of death at the National Forensic Service (NFS), Republic of Korea. The correlation between the concentrations of Hx and l-lactic acid in vitreous humors and PMI was evaluated using 79 corpses (53 males and 26 females), with sampling time ranging from 13 to 103 h after death. The average daily ambient temperature at the time of death of each sample was investigated to calibrate the correlation with PMI. Following correction of the concentrations of Hx and l-lactic acid with temperature, the correlation of Hx and l-lactic acid with PMI increased from 0.53 to 0.59 for Hx and 0.38 to 0.42 for l-lactic acid. The highest correlation of Hx and l-lactic acid concentrations with PMI was observed in the winter season, with an R2 value of 0.80 and 0.71 for Hx and l-lactic acid, respectively. The correlation of Hx and l-lactic acid with PMI was corrected by ambient temperature for each season, resulting in an increase in the R2 value to 0.88 for Hx and 0.72 for l-lactic acid. The best correlation was observed when the temperature was corrected after dividing by season.
Keywords	ambient temperature ; autumn ; biomarkers ; death ; females ; forensic sciences ; humans ; hypoxanthine ; lactic acid ; liquid chromatography ; males ; metabolism ; postmortem changes ; quantitative analysis ; spring ; summer ; tandem mass spectrometry ; winter ; South Korea
Language	English
Dates of publication	2019-06
Size	p. 135-141.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	424042-x
ISSN	1872-6283 ; 0379-0738
ISSN (online)	1872-6283
ISSN	0379-0738
DOI	10.1016/j.forsciint.2019.03.024
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Korean Red Ginseng and Ginsenoside Rg3 Suppress Asian Sand Dust-Induced Epithelial-Mesenchymal Transition in Nasal Epithelial Cells.

Shin, Seung-Heon / Ye, Mi-Kyung / Lee, Dong-Won / Chae, Mi-Hyun / Hwang, You-Jin

Molecules (Basel, Switzerland)

2022 Volume 27, Issue 9

Abstract: Chronic rhinosinusitis (CRS) is characterized by chronic inflammation of the sinonasal mucosa with epithelial dedifferentiation toward the mesenchymal phenotype, known as the epithelial-mesenchymal transition (EMT). Asian sand dust (ASD) can induce nasal ...

Abstract	Chronic rhinosinusitis (CRS) is characterized by chronic inflammation of the sinonasal mucosa with epithelial dedifferentiation toward the mesenchymal phenotype, known as the epithelial-mesenchymal transition (EMT). Asian sand dust (ASD) can induce nasal mucosal inflammation and cause the development of EMT. Korean red ginseng (KRG) and ginsenoside Rg3 have been used as traditional herbal medicines to treat various diseases. The aim of this study was to investigate their effect on ASD-induced EMT in nasal epithelial cells. Primary nasal epithelial cells were incubated with ASD with or without KRG or Rg3, and the production of transforming growth factor-β1 (TGF-β1) and interleukin (IL)-8 was measured. EMT markers were determined by RT-PCR, Western blot analysis, and confocal microscopy, and transcription factor expression by Western blot analysis. The effect on cell migration was evaluated using the wound scratch assay. Results showed ASD-induced TGF-β1 production, downregulation of E-cadherin, and upregulation of fibronectin in nasal epithelial cells. KRG and Rg3 suppressed TGF-β1 production (31.7% to 43.1%), upregulated the expression of E-cadherin (26.4% to 88.3% in mRNA), and downregulated that of fibronectin (14.2% to 46.2% in mRNA and 52.3% to 70.2% in protein). In addition, they suppressed the ASD-induced phosphorylation of ERK, p38, and mTOR, as well as inhibiting the ASD-induced migration of nasal epithelial cells (25.2% to 41.5%). The results of this study demonstrate that KRG and Rg3 inhibit ASD-induced EMT by suppressing the activation of ERK, p38, and mTOR signaling pathways in nasal epithelial cells.
MeSH term(s)	Cadherins/metabolism ; Cell Movement ; Dust ; Epithelial Cells ; Epithelial-Mesenchymal Transition ; Fibronectins/metabolism ; Ginsenosides ; Humans ; Inflammation/metabolism ; Panax/metabolism ; RNA, Messenger/metabolism ; Sand ; TOR Serine-Threonine Kinases/metabolism ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Cadherins ; Dust ; Fibronectins ; Ginsenosides ; RNA, Messenger ; Sand ; Transforming Growth Factor beta1 ; ginsenoside Rg3 (227D367Y57) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-04-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27092642
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