Autophagy-related 5 gene mRNA expression and ATG5 rs510432 polymorphism in children with bronchial asthma.
ATG5
autophagy
childhood bronchial asthma
rs510432 gene polymorphism
Journal
Pediatric pulmonology
ISSN: 1099-0496
Titre abrégé: Pediatr Pulmonol
Pays: United States
ID NLM: 8510590
Informations de publication
Date de publication:
11 2022
11 2022
Historique:
revised:
29
06
2022
received:
09
04
2022
accepted:
09
07
2022
pubmed:
16
7
2022
medline:
19
10
2022
entrez:
15
7
2022
Statut:
ppublish
Résumé
Bronchial asthma is a common chronic respiratory disease in children with complex pathogenesis, characterized by airway hyper-responsiveness, obstruction, mucus hyperproduction, and airway remodeling. Autophagy is important for cellular physiology, and the ATG5 rs510432 has recently been implicated in several fundamental characteristics of childhood asthma pathogenesis and may play a role in the disease progression. This study aims to assess the expression of ATG5 messenger RNA (mRNA) according to rs510432 polymorphism in asthmatic children and to evaluate their possible relation with the development of the disease. ATG5 mRNA expression and rs510432 polymorphism were measured using real-time polymerase chain reaction in 57 asthmatic children patients and 46 healthy controls. ATG5 level was significantly higher in asthmatic children than in controls and a significant increase in the frequency of TT and CC genotype of ATG5 rs510432 gene polymorphism was found in asthmatic patients when compared to control subjects (p < 0.001; and p = 0.01, respectively), and there was a statistically significant decrease in the frequency of CT genotype of ATG5 rs510432 gene polymorphism in asthmatic patients when compared to control subjects (p < 0.001). ATG5 rs510432 gene polymorphism plays an important role in childhood asthma pathogenesis.
Substances chimiques
ATG5 protein, human
0
Autophagy-Related Protein 5
0
RNA, Messenger
0
Cxcl2 protein, mouse
0
Axl Receptor Tyrosine Kinase
0
AXL protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2659-2664Informations de copyright
© 2022 Wiley Periodicals LLC.
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