- VernacularTitle:PRKCQ-AS1通过Akt信号促进气道平滑肌细胞增殖的研究
- Author:
Lu-yi WU
1
;
Fang-qi HU
1
Author Information
- Publication Type:Journal Article
- Keywords: PRKCQ-AS1; ASMCs; asthma; Akt sig-naling; cellular assay; inflammatory cytokines
- From: Chinese Pharmacological Bulletin 2025;41(1):88-94
- CountryChina
- Language:Chinese
- Abstract: Aim To explore the role of PRKCQ-AS1 in airway smooth muscle cells(ASMCs).Methods Differentially expressed genes(DEGs)in alveolar lav-age fluid of children with asthma were first detected by transcriptome sequencing technology(RNA-seq).The expression of PRKCQ-AS1 in ASMCs was detected by qRT-PCR;the proliferation and apoptosis of PRKCQ-AS1 were detected by CCK-8 and flow cytometry,re-spectively;the levels of TNF-α and IL-1β in the cul-ture supernatant of ASMCs were detected by enzyme-linked immunosorbent assay(ELISA);and lncRNA microarray detected DEGs after PRKCQ-AS1 knock-down and KEGG pathway enrichment;Western blot to detect the levels of p-Akt and Akt.Results RNA-seq results showed that PRKCQ-AS1 was one of the most significantly up-regulated DEGs.PRKCQ-AS1 overexpression promoted proliferation and migration and inhibited apoptosis of ASMCs.At the same time,PRKCQ-AS1 overexpression increased the levels of the inflammatory factors TNF-α and IL-1 β in the superna-tant,whereas PRKCQ-AS1 knockdown showed the op-posite results.KEGG signaling pathway enrichment a-nalysis of 606 DEGs obtained after PRKCQ-AS1 knockdown showed that PI3K-Akt signaling was signifi-cantly enriched.Western blot results indicated that PRKCQ-AS1 knockdown inhibited Akt activation;on the contrary,PRKCQ-AS 1 overexpression promoted Akt levels.Conclusions PRKCQ-AS1 promoted the in-flammatory response of ASMCs by enhancing Akt sig-naling probably,which in turn exacerbated the prolifer-ation and migration of ASMCs,ultimately leading to the development of asthma.

