Effect of the CYBA C242T Polymorphism on Preeclampsia Pathogenesis in the Chinese Population.
CYBA C242T polymorphism
Gene expression
HTR-8
Placenta
Preeclampsia
SVneo cells
Journal
Biochemical genetics
ISSN: 1573-4927
Titre abrégé: Biochem Genet
Pays: United States
ID NLM: 0126611
Informations de publication
Date de publication:
04 Sep 2023
04 Sep 2023
Historique:
received:
22
03
2023
accepted:
23
06
2023
medline:
4
9
2023
pubmed:
4
9
2023
entrez:
4
9
2023
Statut:
aheadofprint
Résumé
Although the mechanisms responsible for the pathogenesis of preeclampsia (PE) have not been entirely clarified, oxidative stress is thought to be its leading cause. As a major component responsible for reactive oxygen species (ROS) production during oxidative stress, p22phox, encoded by CYBA, is an essential subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. The aim of this study was to investigate whether CYBA expression and its polymorphism are associated with PE. Expression of CYBA was analysed in placentas from PE and control groups, as well as in HTR-8/SVneo cells stimulated with CoCl2 and TNF-α. Then, the CYBA C242T polymorphism in 1184 patients with PE and 1421 healthy controls was genotyped using the TaqMan probe, and the different distributions identified were confirmed by a case‒control association study. Expression of CYBA mRNA and protein in the placenta of pregnant women with PE was significantly increased compared to controls. Expression of CYBA mRNA was also increased in HTR-8/SVneo cells collected after 24 h of separate stimulation with cobalt chloride and TNF-α. There was no significant difference in the distribution of the C242T locus genotype and CYBA allele frequency between the case group and control group (P > 0.05). CYBA may play a role in the pathogenesis of oxidative stress in PE, in which it may function by cooperating with the TNF-α-related inflammatory pathway. Although no discrepant distribution of the CYBA C242T polymorphism in the Chinese population was detected, it is necessary to examine multiple CYBA SNPs in diverse populations and perform functional experiments to gain further insights into its pathogenesis.
Sections du résumé
BACKGROUND
BACKGROUND
Although the mechanisms responsible for the pathogenesis of preeclampsia (PE) have not been entirely clarified, oxidative stress is thought to be its leading cause. As a major component responsible for reactive oxygen species (ROS) production during oxidative stress, p22phox, encoded by CYBA, is an essential subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. The aim of this study was to investigate whether CYBA expression and its polymorphism are associated with PE.
METHODS
METHODS
Expression of CYBA was analysed in placentas from PE and control groups, as well as in HTR-8/SVneo cells stimulated with CoCl2 and TNF-α. Then, the CYBA C242T polymorphism in 1184 patients with PE and 1421 healthy controls was genotyped using the TaqMan probe, and the different distributions identified were confirmed by a case‒control association study.
RESULTS
RESULTS
Expression of CYBA mRNA and protein in the placenta of pregnant women with PE was significantly increased compared to controls. Expression of CYBA mRNA was also increased in HTR-8/SVneo cells collected after 24 h of separate stimulation with cobalt chloride and TNF-α. There was no significant difference in the distribution of the C242T locus genotype and CYBA allele frequency between the case group and control group (P > 0.05).
CONCLUSIONS
CONCLUSIONS
CYBA may play a role in the pathogenesis of oxidative stress in PE, in which it may function by cooperating with the TNF-α-related inflammatory pathway. Although no discrepant distribution of the CYBA C242T polymorphism in the Chinese population was detected, it is necessary to examine multiple CYBA SNPs in diverse populations and perform functional experiments to gain further insights into its pathogenesis.
Identifiants
pubmed: 37665479
doi: 10.1007/s10528-023-10440-7
pii: 10.1007/s10528-023-10440-7
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Natural Science Fund Project of Shandong Province
ID : ZR2019MH127
Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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