1.Role of NEAT1/MiR-9-5p/SLC26A2 Pathway on Human Airway Smooth Muscle Cell
Xiangying WANG ; Ruju XU ; Di CHI ; Chufeng DAI ; Meiling SHENG
Yonsei Medical Journal 2021;62(9):858-867
Purpose:
Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs.
Materials and Methods:
We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses.
Results:
SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs.
Conclusion
These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.
2.Role of NEAT1/MiR-9-5p/SLC26A2 Pathway on Human Airway Smooth Muscle Cell
Xiangying WANG ; Ruju XU ; Di CHI ; Chufeng DAI ; Meiling SHENG
Yonsei Medical Journal 2021;62(9):858-867
Purpose:
Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs.
Materials and Methods:
We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses.
Results:
SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs.
Conclusion
These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.
3.Effect of doxycycline administered at different times on macrolide-resistant children with Mycoplasma pneumoniae pneumonia
Chufeng DAI ; Fang ZHOU ; Qin HUANG ; Qimin SHAO
China Pharmacist 2024;28(11):431-437
Objective To evaluate the impact of different dosing times of doxycycline(DOX)on children with macrolide-resistant Mycoplasma pneumoniae pneumonia(MR-MPP).Methods Clinical data of children diagnosed with MR-MPP at Hangzhou Children's Hospital from January 2022 to December 2023 were analyzed.Children were divided into three groups based on treatment regimens:the doxycycline(DOX)group,the intravenous azithromycin converted to oral DOX(ATD)group,and the intravenous azithromycin alone(AZI)group..The ATD group was further divided into ATD1 group(<3 days)and ATD2 group(>3 days)according to the duration of azithromycin treatment.Clinical symptoms of each group were compared,and propensity score matching(PSM)analysis was used for adjustment.Results A total of 156 children with MR-MPP were included in the study,with 25 in the DOX group,85 in the ATD group,and 46 in the AZI group.Compared with the ATD and AZI groups,the DOX group had a shorter hospital stay and fever duration,higher chest radiograph improvement rate,and lower glucocorticoid usage rate(P<0.05).The DOX group and ATD1 group had lower hospital stays,post-treatment fever durations,and glucocorticoid usage rates than the ATD2 group,and higher 96-hour fever resolution rates and chest X-ray improvement rates than the ATD2 group(P<0.05).The DOX group had a higher fever resolution rate within 72 hours compared to the ATD1 and ATD2 groups(P<0.05).PSM analysis showed that the DOX-ATD1 group had a lower hospital stay,post-treatment fever duration,and glucocorticoid usage rate than the ATD2 group,and a higher 72-hour fever resolution rate than the ATD2 group(all P<0.05).No adverse reactions related to DOX were observed during the treatment period.Conclusion Early oral administration of DOX within 72 hours can significantly improve the clinical efficacy in children with MR-MPP.