Effects of Drugs Formerly Proposed for COVID-19 Treatment on Connexin43 Hemichannels.
COVID-19
cellular communication
connexin43
drug
hemichannel
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
30 Apr 2022
30 Apr 2022
Historique:
received:
19
04
2022
revised:
26
04
2022
accepted:
26
04
2022
entrez:
14
5
2022
pubmed:
15
5
2022
medline:
18
5
2022
Statut:
epublish
Résumé
Connexin43 (Cx43) hemichannels form a pathway for cellular communication between the cell and its extracellular environment. Under pathological conditions, Cx43 hemichannels release adenosine triphosphate (ATP), which triggers inflammation. Over the past two years, azithromycin, chloroquine, dexamethasone, favipiravir, hydroxychloroquine, lopinavir, remdesivir, ribavirin, and ritonavir have been proposed as drugs for the treatment of the coronavirus disease 2019 (COVID-19), which is associated with prominent systemic inflammation. The current study aimed to investigate if Cx43 hemichannels, being key players in inflammation, could be affected by these drugs which were formerly designated as COVID-19 drugs. For this purpose, Cx43-transduced cells were exposed to these drugs. The effects on Cx43 hemichannel activity were assessed by measuring extracellular ATP release, while the effects at the transcriptional and translational levels were monitored by means of real-time quantitative reverse transcriptase polymerase chain reaction analysis and immunoblot analysis, respectively. Exposure to lopinavir and ritonavir combined (4:1 ratio), as well as to remdesivir, reduced Cx43 mRNA levels. None of the tested drugs affected Cx43 protein expression.
Identifiants
pubmed: 35563409
pii: ijms23095018
doi: 10.3390/ijms23095018
pmc: PMC9103705
pii:
doi:
Substances chimiques
Connexin 43
0
Lopinavir
2494G1JF75
Adenosine Triphosphate
8L70Q75FXE
Ritonavir
O3J8G9O825
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Research Foundation Flanders-Belgium
Organisme : Scientific Fund Willy Gepts-Belgium
Organisme : Methusalem program of the Flemish government
Organisme : European Research Council
ID : Proof-of-Concept Grant 861913
Pays : International
Organisme : European Commission
ID : FETopen Grant 858014
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