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  1. AU="Juan Prieto-Villalobos"
  2. AU="Blot, Guillaume"
  3. AU="Sanchez, Gabriela"
  4. AU=Mitton Julian A
  5. AU="Han, Hyunho"
  6. AU="Shama, Noura M Abo"
  7. AU=Uehara Akira
  8. AU=Fransen Justin H AU=Fransen Justin H
  9. AU="Memon, Roha Saeed"
  10. AU="Lipworth, Samuel"
  11. AU="Killian, Michael O"
  12. AU=Smaldino Paul E.
  13. AU=Bi Hai
  14. AU="Pintore, Giorgio"
  15. AU="Signorini C."
  16. AU="Mameli, Maria Sabrina"
  17. AU="Yong-ming GAO"
  18. AU="Paquette, Kimberly"
  19. AU="Sharawat, Indar Kumar"
  20. AU="Alexandre Alanio"
  21. AU="Caron, Jeffrey G"
  22. AU="Lubisi, Baratang A"
  23. AU="Edelman, Robert R."
  24. AU="van der Werf, Steffie"
  25. AU="Sam, Andrew"

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  1. Artikel ; Online: SARS-CoV-2 spike protein S1 activates Cx43 hemichannels and disturbs intracellular Ca2+ dynamics

    Juan Prieto-Villalobos / Claudia M. Lucero / Maximiliano Rovegno / Gonzalo I. Gómez / Mauricio A. Retamal / Juan A. Orellana

    Biological Research, Vol 56, Iss 1, Pp 1-

    2023  Band 14

    Abstract: Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the ongoing coronavirus disease 2019 (COVID-19). An aspect of high uncertainty is whether the SARS-CoV-2 per se or the systemic inflammation induced by viral ... ...

    Abstract Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the ongoing coronavirus disease 2019 (COVID-19). An aspect of high uncertainty is whether the SARS-CoV-2 per se or the systemic inflammation induced by viral infection directly affects cellular function and survival in different tissues. It has been postulated that tissue dysfunction and damage observed in COVID-19 patients may rely on the direct effects of SARS-CoV-2 viral proteins. Previous evidence indicates that the human immunodeficiency virus and its envelope protein gp120 increase the activity of connexin 43 (Cx43) hemichannels with negative repercussions for cellular function and survival. Here, we evaluated whether the spike protein S1 of SARS-CoV-2 could impact the activity of Cx43 hemichannels. Results We found that spike S1 time and dose-dependently increased the activity of Cx43 hemichannels in HeLa-Cx43 cells, as measured by dye uptake experiments. These responses were potentiated when the angiotensin-converting enzyme 2 (ACE2) was expressed in HeLa-Cx43 cells. Patch clamp experiments revealed that spike S1 increased unitary current events with conductances compatible with Cx43 hemichannels. In addition, Cx43 hemichannel opening evoked by spike S1 triggered the release of ATP and increased the [Ca2+]i dynamics elicited by ATP. Conclusions We hypothesize that Cx43 hemichannels could represent potential pharmacological targets for developing therapies to counteract SARS-CoV-2 infection and their long-term consequences.
    Schlagwörter Hemichannels ; COVID-19 ; Connexin 43 ; SARS-CoV-2 ; ACE2 ; ATP and spike S1 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2023-10-01T00:00:00Z
    Verlag BMC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: GABAergic Regulation of Astroglial Gliotransmission through Cx43 Hemichannels

    Ivanka Jiménez-Dinamarca / Rachel Reyes-Lizana / Yordan Lemunao-Inostroza / Kevin Cárdenas / Raimundo Castro-Lazo / Francisca Peña / Claudia M. Lucero / Juan Prieto-Villalobos / Mauricio Antonio Retamal / Juan Andrés Orellana / Jimmy Stehberg

    International Journal of Molecular Sciences, Vol 23, Iss 13625, p

    2022  Band 13625

    Abstract: Gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain. It is produced by interneurons and recycled by astrocytes. In neurons, GABA activates the influx of Cl - via the GABA A receptor or efflux or K + via the GABA B ... ...

    Abstract Gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain. It is produced by interneurons and recycled by astrocytes. In neurons, GABA activates the influx of Cl - via the GABA A receptor or efflux or K + via the GABA B receptor, inducing hyperpolarization and synaptic inhibition. In astrocytes, the activation of both GABA A and GABA B receptors induces an increase in intracellular Ca 2+ and the release of glutamate and ATP. Connexin 43 (Cx43) hemichannels are among the main Ca 2+ -dependent cellular mechanisms for the astroglial release of glutamate and ATP. However, no study has evaluated the effect of GABA on astroglial Cx43 hemichannel activity and Cx43 hemichannel-mediated gliotransmission. Here we assessed the effects of GABA on Cx43 hemichannel activity in DI NCT1 rat astrocytes and hippocampal brain slices. We found that GABA induces a Ca 2+ -dependent increase in Cx43 hemichannel activity in astrocytes mediated by the GABA A receptor, as it was blunted by the GABA A receptor antagonist bicuculline but unaffected by GABA B receptor antagonist CGP55845. Moreover, GABA induced the Cx43 hemichannel-dependent release of glutamate and ATP, which was also prevented by bicuculline, but unaffected by CGP. Gliotransmission in response to GABA was also unaffected by pannexin 1 channel blockade. These results are discussed in terms of the possible role of astroglial Cx43 hemichannel-mediated glutamate and ATP release in regulating the excitatory/inhibitory balance in the brain and their possible contribution to psychiatric disorders.
    Schlagwörter GABA ; GABA A receptors ; astrocytes ; Cx43 hemichannels ; astroglia ; connexin 43 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 333
    Sprache Englisch
    Erscheinungsdatum 2022-11-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: TNF-α Plus IL-1β Induces Opposite Regulation of Cx43 Hemichannels and Gap Junctions in Mesangial Cells through a RhoA/ROCK-Dependent Pathway

    Claudia M. Lucero / Lucas Marambio-Ruiz / Javiera Balmazabal / Juan Prieto-Villalobos / Marcelo León / Paola Fernández / Juan A. Orellana / Victoria Velarde / Juan C. Sáez / Gonzalo I. Gómez

    International Journal of Molecular Sciences, Vol 23, Iss 10097, p

    2022  Band 10097

    Abstract: Connexin 43 (Cx43) is expressed in kidney tissue where it forms hemichannels and gap junction channels. However, the possible functional relationship between these membrane channels and their role in damaged renal cells remains unknown. Here, analysis of ...

    Abstract Connexin 43 (Cx43) is expressed in kidney tissue where it forms hemichannels and gap junction channels. However, the possible functional relationship between these membrane channels and their role in damaged renal cells remains unknown. Here, analysis of ethidium uptake and thiobarbituric acid reactive species revealed that treatment with TNF-α plus IL-1β increases Cx43 hemichannel activity and oxidative stress in MES-13 cells (a cell line derived from mesangial cells), and in primary mesangial cells. The latter was also accompanied by a reduction in gap junctional communication, whereas Western blotting assays showed a progressive increase in phosphorylated MYPT (a target of RhoA/ROCK) and Cx43 upon TNF-α/IL-1β treatment. Additionally, inhibition of RhoA/ROCK strongly antagonized the TNF-α/IL-1β-induced activation of Cx43 hemichannels and reduction in gap junctional coupling. We propose that activation of Cx43 hemichannels and inhibition of cell–cell coupling during pro-inflammatory conditions could contribute to oxidative stress and damage of mesangial cells via the RhoA/ROCK pathway.
    Schlagwörter connexin hemichannel ; gap junction ; oxidative stress ; inflammatory receptors ; Fasudil ; Y-27632 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2022-09-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Astroglial Hemichannels and Pannexons

    Juan Prieto-Villalobos / Tanhia F. Alvear / Andrés Liberona / Claudia M. Lucero / Claudio J. Martínez-Araya / Javiera Balmazabal / Carla A. Inostroza / Gigliola Ramírez / Gonzalo I. Gómez / Juan A. Orellana

    International Journal of Molecular Sciences, Vol 22, Iss 9503, p

    The Hidden Link between Maternal Inflammation and Neurological Disorders

    2021  Band 9503

    Abstract: Maternal inflammation during pregnancy causes later-in-life alterations of the offspring’s brain structure and function. These abnormalities increase the risk of developing several psychiatric and neurological disorders, including schizophrenia, ... ...

    Abstract Maternal inflammation during pregnancy causes later-in-life alterations of the offspring’s brain structure and function. These abnormalities increase the risk of developing several psychiatric and neurological disorders, including schizophrenia, intellectual disability, bipolar disorder, autism spectrum disorder, microcephaly, and cerebral palsy. Here, we discuss how astrocytes might contribute to postnatal brain dysfunction following maternal inflammation, focusing on the signaling mediated by two families of plasma membrane channels: hemi-channels and pannexons. [Ca 2+ ] i imbalance linked to the opening of astrocytic hemichannels and pannexons could disturb essential functions that sustain astrocytic survival and astrocyte-to-neuron support, including energy and redox homeostasis, uptake of K + and glutamate, and the delivery of neurotrophic factors and energy-rich metabolites. Both phenomena could make neurons more susceptible to the harmful effect of prenatal inflammation and the experience of a second immune challenge during adulthood. On the other hand, maternal inflammation could cause excitotoxicity by producing the release of high amounts of gliotransmitters via astrocytic hemichannels/pannexons, eliciting further neuronal damage. Understanding how hemichannels and pannexons participate in maternal inflammation-induced brain abnormalities could be critical for developing pharmacological therapies against neurological disorders observed in the offspring.
    Schlagwörter connexins ; pannexins ; hemichannels ; pannexons ; neuroinflammation ; lipopolysaccharide ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Sprache Englisch
    Erscheinungsdatum 2021-09-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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