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  1. Article ; Online: SARS-CoV-2, More than a Respiratory Virus: Its Potential Role in Neuropathogenesis.

    Singal, Chitra Mohinder Singh / Jaiswal, Paritosh / Seth, Pankaj

    ACS chemical neuroscience

    2020  Volume 11, Issue 13, Page(s) 1887–1899

    Abstract: The coronavirus disease-19 (COVID-19) pandemic has emerged as one of the major outbreaks to be mentioned in history in coming times. Like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), severe acute respiratory ... ...

    Abstract The coronavirus disease-19 (COVID-19) pandemic has emerged as one of the major outbreaks to be mentioned in history in coming times. Like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a respiratory virus infecting the lungs with fever, dry cough, and acute pneumonia being the major symptoms. It infects epithelial cells expressing angiotensin converting enzyme 2 (ACE2) receptor, which is crucial for viral entry. Based on evolving clinical evidence, it is now unfitting to label SARS-CoV-2 as just a respiratory virus, as lately there are various reports that substantiate its pathogenicity in other organs of the body, including brain. In this review, we discuss the epidemiology of SARS-CoV-2 in comparison to SARS and MERS along with possibilities of viral entry into central nervous system (CNS) tissues. The review provides detailed information about the virulence, epidemiology, and insights into molecular pathways involved in the infectivity of the SARS-CoV-2 virus, along with an in-depth view of current concepts about the neurological significance of the SARS-CoV-2 virus and its neuropathological competence. The review also touches upon our current understanding of placental transmission of SARS-CoV-2, an important aspect of vertical transmission. Furthermore, the review provides a current update on strategies that have been used, are being used, or are under trial for treating the disease.
    MeSH term(s) Angiotensin-Converting Enzyme 2 ; Betacoronavirus/metabolism ; Brain/metabolism ; Brain/pathology ; Brain/virology ; COVID-19 ; Coronavirus Infections/epidemiology ; Coronavirus Infections/metabolism ; Coronavirus Infections/pathology ; Humans ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neurodegenerative Diseases/virology ; Pandemics ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/metabolism ; Pneumonia, Viral/pathology ; SARS-CoV-2 ; Severe Acute Respiratory Syndrome/epidemiology ; Severe Acute Respiratory Syndrome/metabolism ; Severe Acute Respiratory Syndrome/pathology
    Chemical Substances Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Keywords covid19
    Language English
    Publishing date 2020-06-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1948-7193
    ISSN (online) 1948-7193
    DOI 10.1021/acschemneuro.0c00251
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  2. Article ; Online: SARS-CoV-2, More than a Respiratory Virus

    Singal, Chitra Mohinder Singh / Jaiswal, Paritosh / Seth, Pankaj

    ACS Chemical Neuroscience

    Its Potential Role in Neuropathogenesis

    2020  Volume 11, Issue 13, Page(s) 1887–1899

    Keywords Cell Biology ; Biochemistry ; Physiology ; Cognitive Neuroscience ; General Medicine ; covid19
    Language English
    Publisher American Chemical Society (ACS)
    Publishing country us
    Document type Article ; Online
    ISSN 1948-7193
    DOI 10.1021/acschemneuro.0c00251
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Role of EphrinA3 in HIV-1 Neuropathogenesis.

    Singal, Chitra Mohinder Singh / Jaiswal, Paritosh / Mehta, Anuradha / Saleem, Kanza / Seth, Pankaj

    ASN neuro

    2021  Volume 13, Page(s) 17590914211044359

    Abstract: Glial cells perform important supporting functions for neurons through a dynamic crosstalk. Neuron-glia communication is the major phenomenon to sustain homeostatic functioning of the brain. Several interactive pathways between neurons and astrocytes are ...

    Abstract Glial cells perform important supporting functions for neurons through a dynamic crosstalk. Neuron-glia communication is the major phenomenon to sustain homeostatic functioning of the brain. Several interactive pathways between neurons and astrocytes are critical for the optimal functioning of neurons, and one such pathway is the ephrinA3-ephA4 signaling. The role of this pathway is essential in maintaining the levels of extracellular glutamate by regulating the excitatory amino acid transporters, EAAT1 and EAAT2 on astrocytes. Human immunodeficiency virus-1 (HIV-1) and its proteins cause glutamate excitotoxicity due to excess glutamate levels at sites of high synaptic activity. This study unravels the effects of HIV-1 transactivator of transcription (Tat) from clade B on ephrinA3 and its role in regulating glutamate levels in astrocyte-neuron co-cultures of human origin. It was observed that the expression of ephrinA3 increases in the presence of HIV-1 Tat B, while the expression of EAAT1 and EAAT2 was attenuated. This led to reduced glutamate uptake and therefore high neuronal death due to glutamate excitotoxicity. Knockdown of ephrinA3 using small interfering RNA, in the presence of HIV-1 Tat B reversed the neurotoxic effects of HIV-1 Tat B via increased expression of glutamate transporters that reduced the levels of extracellular glutamate. The in vitro findings were validated in autopsy brain sections from acquired immunodeficiency syndrome patients and we found ephrinA3 to be upregulated in the case of HIV-1-infected patients. This study offers valuable insights into astrocyte-mediated neuronal damage in HIV-1 neuropathogenesis.
    MeSH term(s) Astrocytes/metabolism ; Ephrin-A3 ; Excitatory Amino Acid Transporter 2/metabolism ; Glutamic Acid ; HIV-1/metabolism ; Humans ; Neurons/metabolism ; Signal Transduction
    Chemical Substances Ephrin-A3 ; Excitatory Amino Acid Transporter 2 ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2021-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2485467-0
    ISSN 1759-0914 ; 1759-0914
    ISSN (online) 1759-0914
    ISSN 1759-0914
    DOI 10.1177/17590914211044359
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Sinomenine inhibits amyloid beta-induced astrocyte activation and protects neurons against indirect toxicity.

    Singh, Deepali / Agrawal, Apurva / Singal, Chitra Mohinder Singh / Pandey, Hriday Shanker / Seth, Pankaj / Sharma, Shiv Kumar

    Molecular brain

    2020  Volume 13, Issue 1, Page(s) 30

    Abstract: Amyloid beta is a major constituent of the plaques found in the brains of patients suffering from Alzheimer's disease (AD). A growing body of research work suggests that neuroinflammation plays important roles in the development of AD. Thus, considerable ...

    Abstract Amyloid beta is a major constituent of the plaques found in the brains of patients suffering from Alzheimer's disease (AD). A growing body of research work suggests that neuroinflammation plays important roles in the development of AD. Thus, considerable efforts are directed towards identification of compounds that can reduce or inhibit neuroinflammation. Here, we show that sinomenine, a compound present in a Chinese medicinal plant, Sinomenium acutum, inhibits oligomeric amyloid beta-induced production of reactive oxygen species (ROS), nitric oxide (NO) and inflammation-related molecules from astrocytic cells. The conditioned medium from oligomeric amyloid beta-treated astrocytic cells induces cell death in the hippocampal neuronal cells. Importantly, sinomenine inhibits this cell death. In addition, this compound has inhibitory effects on the production of ROS, NO and inflammation-related factors from oligomeric amyloid-beta treated human astrocytes. Finally, the conditioned medium from oligomeric amyloid beta-treated human astrocytes induces cell death in the primary culture of human neurons, which is inhibited by sinomenine. Thus, sinomenine inhibits amyloid beta-induced production of toxic factors from astrocytes, and confers protection to hippocampal neuronal cells as well as human neurons against indirect toxicity. The results suggest that this compound could provide beneficial effects in AD and other neurodegenerative conditions by reducing inflammation and neuronal cell death.
    MeSH term(s) Amyloid beta-Peptides/toxicity ; Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Astrocytes/pathology ; Cell Line ; Hippocampus/pathology ; Humans ; Inflammation/pathology ; Mice ; Morphinans/pharmacology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Neuroprotective Agents/pharmacology ; Nitric Oxide/metabolism ; Reactive Oxygen Species/metabolism
    Chemical Substances Amyloid beta-Peptides ; Morphinans ; Neuroprotective Agents ; Reactive Oxygen Species ; Nitric Oxide (31C4KY9ESH) ; sinomenine (63LT81K70N)
    Language English
    Publishing date 2020-03-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2436057-0
    ISSN 1756-6606 ; 1756-6606
    ISSN (online) 1756-6606
    ISSN 1756-6606
    DOI 10.1186/s13041-020-00569-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Hypoxia Induces Early Neurogenesis in Human Fetal Neural Stem Cells by Activating the WNT Pathway.

    Dey, Devanjan / Shrivastava, Vadanya / Joshi, Diksha / Singal, Chitra Mohinder Singh / Tyagi, Sagar / Bhat, Muzaffer Ahmed / Jaiswal, Paritosh / Sharma, Jai Bhagwan / Palanichamy, Jayanth Kumar / Sinha, Subrata / Seth, Pankaj / Sen, Sudip

    Molecular neurobiology

    2023  Volume 60, Issue 5, Page(s) 2910–2921

    Abstract: Fetal neural stem cells (FNSCs) present in the human fetal brain differentiate into cells of neuronal and glial lineages. The developing fetus is exposed to lower oxygen concentrations than adults, and this physiological hypoxia may influence the growth ... ...

    Abstract Fetal neural stem cells (FNSCs) present in the human fetal brain differentiate into cells of neuronal and glial lineages. The developing fetus is exposed to lower oxygen concentrations than adults, and this physiological hypoxia may influence the growth and differentiation of the FNSCs. This study aimed to evaluate the effect of hypoxia on the differentiation potential of human FNSCs isolated from the subventricular zone of aborted fetal brains (n = 5). FNSCs were isolated, expanded, and characterized by Nestin and Sox2 expression using immunocytochemistry and flow cytometry, respectively. These FNSCs were exposed to 20% oxygen (normoxia) and 0.2% oxygen (hypoxia) concentrations for 48 h, and hypoxia exposure (n = 5) was validated. Whole transcriptome analyses (Genespring GX13) of FNSCs exposed to hypoxia (Agilent 4 × 44 K human array slides) highlighted that genes associated with neurogenesis were enriched upon exposure to hypoxia. The pathway analysis of these enriched genes (using Metacore) showed the involvement of the WNT signaling pathway. Microarray analyses were validated using neuronal and glial lineage commitment markers, namely, NEUROG1, NEUROG2, ASCL1, DCX, GFAP, OLIG2, and NKX2.2, using qPCR (n = 9). DCX, ASCL1, NGN1, and GFAP protein expression was analyzed by Western blotting (n = 3). This demonstrated upregulation of the neuronal commitment markers upon hypoxia exposure, while no change was observed in astrocytic and oligodendrocyte lineage commitment markers. Increased expression of downstream targets of the WNT signaling pathway, TCF4 and ID2, by qPCR (n = 9) and increased protein expression of CTNNB1 (β-catenin) and ID2 by Western blot (n = 3) indicated its involvement in mediating neuronal differentiation upon exposure to hypoxia.
    MeSH term(s) Humans ; Wnt Signaling Pathway ; Cells, Cultured ; Neural Stem Cells/metabolism ; Neurogenesis ; Cell Differentiation ; Fetus ; Hypoxia/metabolism ; Oxygen/pharmacology ; Oxygen/metabolism
    Chemical Substances Oxygen (S88TT14065)
    Language English
    Publishing date 2023-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03248-4
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  6. Article: SARS-CoV-2, More than a Respiratory Virus: Its Potential Role in Neuropathogenesis

    Singal, Chitra Mohinder Singh / Jaiswal, Paritosh / Seth, Pankaj

    ACS Chem Neurosci

    Abstract: The coronavirus disease-19 (COVID-19) pandemic has emerged as one of the major outbreaks to be mentioned in history in coming times. Like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), severe acute respiratory ... ...

    Abstract The coronavirus disease-19 (COVID-19) pandemic has emerged as one of the major outbreaks to be mentioned in history in coming times. Like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a respiratory virus infecting the lungs with fever, dry cough, and acute pneumonia being the major symptoms. It infects epithelial cells expressing angiotensin converting enzyme 2 (ACE2) receptor, which is crucial for viral entry. Based on evolving clinical evidence, it is now unfitting to label SARS-CoV-2 as just a respiratory virus, as lately there are various reports that substantiate its pathogenicity in other organs of the body, including brain. In this review, we discuss the epidemiology of SARS-CoV-2 in comparison to SARS and MERS along with possibilities of viral entry into central nervous system (CNS) tissues. The review provides detailed information about the virulence, epidemiology, and insights into molecular pathways involved in the infectivity of the SARS-CoV-2 virus, along with an in-depth view of current concepts about the neurological significance of the SARS-CoV-2 virus and its neuropathological competence. The review also touches upon our current understanding of placental transmission of SARS-CoV-2, an important aspect of vertical transmission. Furthermore, the review provides a current update on strategies that have been used, are being used, or are under trial for treating the disease.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #505648
    Database COVID19

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  7. Article ; Online: Glutamate Uptake Is Not Impaired by Hypoxia in a Culture Model of Human Fetal Neural Stem Cell-Derived Astrocytes.

    Shrivastava, Vadanya / Dey, Devanjan / Singal, Chitra Mohinder Singh / Jaiswal, Paritosh / Singh, Ankit / Sharma, Jai Bhagwan / Chattopadhyay, Parthaprasad / Nayak, Nihar Ranjan / Palanichamy, Jayanth Kumar / Sinha, Subrata / Seth, Pankaj / Sen, Sudip

    Genes

    2022  Volume 13, Issue 3

    Abstract: Hypoxic ischemic injury to the fetal and neonatal brain is a leading cause of death and disability worldwide. Although animal and culture studies suggest that glutamate excitotoxicity is a primary contributor to neuronal death following hypoxia, the ... ...

    Abstract Hypoxic ischemic injury to the fetal and neonatal brain is a leading cause of death and disability worldwide. Although animal and culture studies suggest that glutamate excitotoxicity is a primary contributor to neuronal death following hypoxia, the molecular mechanisms, and roles of various neural cells in the development of glutamate excitotoxicity in humans, is not fully understood. In this study, we developed a culture model of human fetal neural stem cell (FNSC)-derived astrocytes and examined their glutamate uptake in response to hypoxia. We isolated, established, and characterized cultures of FNSCs from aborted fetal brains and differentiated them into astrocytes, characterized by increased expression of the astrocyte markers glial fibrillary acidic protein (GFAP), excitatory amino acid transporter 1 (EAAT1) and EAAT2, and decreased expression of neural stem cell marker Nestin. Differentiated astrocytes were exposed to various oxygen concentrations mimicking normoxia (20% and 6%), moderate and severe hypoxia (2% and 0.2%, respectively). Interestingly, no change was observed in the expression of the glutamate transporter EAAT2 or glutamate uptake by astrocytes, even after exposure to severe hypoxia for 48 h. These results together suggest that human FNSC-derived astrocytes can maintain glutamate uptake after hypoxic injury and thus provide evidence for the possible neuroprotective role of astrocytes in hypoxic conditions.
    MeSH term(s) Astrocytes/metabolism ; Cell Hypoxia ; Cells, Cultured ; Excitatory Amino Acid Transporter 1/genetics ; Excitatory Amino Acid Transporter 1/metabolism ; Glutamic Acid/metabolism ; Humans ; Neural Stem Cells/metabolism
    Chemical Substances Excitatory Amino Acid Transporter 1 ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2022-03-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes13030506
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  8. Article: Glutamate Uptake Is Not Impaired by Hypoxia in a Culture Model of Human Fetal Neural Stem Cell-Derived Astrocytes

    Shrivastava, Vadanya / Dey, Devanjan / Singal, Chitra Mohinder Singh / Jaiswal, Paritosh / Singh, Ankit / Sharma, Jai Bhagwan / Chattopadhyay, Parthaprasad / Nayak, Nihar Ranjan / Palanichamy, Jayanth Kumar / Sinha, Subrata / Seth, Pankaj / Sen, Sudip

    Genes. 2022 Mar. 12, v. 13, no. 3

    2022  

    Abstract: Hypoxic ischemic injury to the fetal and neonatal brain is a leading cause of death and disability worldwide. Although animal and culture studies suggest that glutamate excitotoxicity is a primary contributor to neuronal death following hypoxia, the ... ...

    Abstract Hypoxic ischemic injury to the fetal and neonatal brain is a leading cause of death and disability worldwide. Although animal and culture studies suggest that glutamate excitotoxicity is a primary contributor to neuronal death following hypoxia, the molecular mechanisms, and roles of various neural cells in the development of glutamate excitotoxicity in humans, is not fully understood. In this study, we developed a culture model of human fetal neural stem cell (FNSC)-derived astrocytes and examined their glutamate uptake in response to hypoxia. We isolated, established, and characterized cultures of FNSCs from aborted fetal brains and differentiated them into astrocytes, characterized by increased expression of the astrocyte markers glial fibrillary acidic protein (GFAP), excitatory amino acid transporter 1 (EAAT1) and EAAT2, and decreased expression of neural stem cell marker Nestin. Differentiated astrocytes were exposed to various oxygen concentrations mimicking normoxia (20% and 6%), moderate and severe hypoxia (2% and 0.2%, respectively). Interestingly, no change was observed in the expression of the glutamate transporter EAAT2 or glutamate uptake by astrocytes, even after exposure to severe hypoxia for 48 h. These results together suggest that human FNSC-derived astrocytes can maintain glutamate uptake after hypoxic injury and thus provide evidence for the possible neuroprotective role of astrocytes in hypoxic conditions.
    Keywords amino acid transporters ; astrocytes ; brain ; death ; glutamic acid ; humans ; hypoxia ; models ; neural stem cells ; neurons ; neuroprotective effect ; normoxia ; oxygen
    Language English
    Dates of publication 2022-0312
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes13030506
    Database NAL-Catalogue (AGRICOLA)

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