Pneumonia is a lower respiratory disease caused by pathogens or other factors. This study aimed to explore the roles and mechanism of long noncoding RNA HAGLROS in lipopolysaccharides (LPS)-induced inflammatory injury in pneumonia. The HAGLROS expression in serum of patients with acute stage pneumonia was detected. To induce pulmonary injury, WI-38 human lung fibroblasts were stimulated with lipopolysaccharides (LPS). The HAGLROS expressions in LPS-treated WI-38 cells and the effects of HAGLROS knockdown on the viability, apoptosis, and autophagy of LPS-induced cells were detected. Moreover, the regulatory relationship between HAGLROS and miR-100 was explored as well as the functional targets of miR-100 were identified. Furthermore, the regulatory relationship between miR-100 and PI3K/AKT/NF-κB pathway was elucidated. LncRNA HAGLROS was higher expressed in serum of patients with acute stage pneumonia compared with that in serum of healthy control. LPS caused WI-38 cell injury and increased HAGLROS levels. Downregulation of HAGLROS alleviated LPS-induced cell injury via increasing cell viability, and inhibiting apoptosis and autophagy. Moreover, there was a negative correlation between HAGLROS and miR-100, and the effects of HAGLROS downregulation on LPS-induced apoptosis and autophagy in WI-38 cells were by regulation of miR-100. Furthermore, NFΚB3 was verified as a functional target of miR-100 and effects of miR-100 inhibition on LPS-induced WI-38 cell injury were alleviated by knockdown of NFΚB3. Besides, Knockdown of HAGLROS inhibited the activation of PI3K/AKT/NF-κB pathway. Our findings reveal that downregulation of HAGLROS may alleviate LPS-induced inflammatory injury in WI-38 cells via modulating miR-100/NF-κB axis. HAGLROS/miR-100/NF-κB axis may provide a new strategy for treating acute stage of pneumonia.
Rupture of atherosclerotic plaques constitutes the major cause of thrombosis and acute ischemic coronary syndrome. Bone marrow‐derived mesenchymal stem cells microvesicles (BMSCs‐MVs) are reported to promote angiogenesis. This study investigated the role of BMSCs‐MVs in stabilizing atherosclerotic plaques. BMSCs‐MVs in mice were isolated and identified. The mouse model of atherosclerosis was established, and mice were injected with BMSCs‐MVs via the tail vein. The macrophage model with high glucose and oxidative damage was established and then incubated with BMSCs‐MVs. Nod‐like receptor protein 3 (NLRP3) expression, pyroptosis‐related proteins, and inflammatory factors were detected. Actinomycin D was used to inhibit the secretion of BMSCs‐MVs to verify the source of microRNA‐223 (miR‐223). The binding relationship between miR‐223 and NLRP3 was predicted and verified. BMSCs‐MVs with knockdown of miR‐223 were cocultured with bone marrow‐derived macrophages with knockdown of NLRP3, and then levels of miR‐223, NLRP3, pyroptosis‐related proteins, and inflammatory factors were detected. BMSCs‐MVs could reduce the vulnerability index of atherosclerotic plaques and intima‐media thickness in mice, and inhibit pyroptosis and inflammation. BMSCs‐MVs inhibited pyroptosis and inflammatory factors in macrophages. BMSCs‐MVs carried miR‐223 to inhibit NLRP3 expression and reduce macrophage pyroptosis, thereby stabilizing the atherosclerotic plaques.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.