Downregulation of circ_0035292 Alleviates LPS-Induced WI-38 Cell Injury via Targeting miR-494-3p/TLR4 Pathway in Infantile Pneumonia

Dai, Zhenzhao; Hu, Jianhui; Luo, Zhicheng; Xiao, Jing

doi:10.1007/s10528-023-10455-0

Cited by 1 publication

(2 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, miR-30b-5p inhibits TLR4 activity, decreasing the expression of pro-inflammatory molecules including VCAM-1, ICAM-1, TNF-α, NFκB, and p38 in ECs 29,30 . Previous studies have demonstrated that miR-494-3p has multifaceted therapeutic potentials across various pathological conditions, including inflammatory responses, oxidative stress pathways, and angiogenesis 31-33 . Interestingly, in WI-38 cells, miR-494 directly interacts with TLR4 and regulates oxidative stress 31 .…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have demonstrated that miR-494-3p has multifaceted therapeutic potentials across various pathological conditions, including inflammatory responses, oxidative stress pathways, and angiogenesis 31-33 . Interestingly, in WI-38 cells, miR-494 directly interacts with TLR4 and regulates oxidative stress 31 . This evidence supports the potential of these miRNAs as future novel therapeutics.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Human Breast Milk EVs Mitigate Endothelial Dysfunction: Preliminary Study

Cho,

Chen,

Crouch

et al. 2024

Preprint

View full text Add to dashboard Cite

Background: Endothelial cell (EC) dysfunction is an early indicator of failing vascular integrity, leading to various cardiovascular diseases. Toll-like receptor 4 (TLR4) activation is a key mechanism. Milk-derived extracellular vesicles (EVs) are known for their anti-inflammatory properties, particularly in suppressing TLR4 activation in damaged intestinal epithelial cells. This study explores the therapeutic potential of human breast milk EVs (bEVs) in EC dysfunction related to cardiovascular diseases. Methods: Human breast milk EVs (bEVs) were isolated from healthy nursing mothers using ultracentrifugation. bEVs were applied to LPS-treated HUVECs, and the expression of inflammatory markers was measured using qPCR and western blotting. Angiogenesis was assessed via a wound assay. Additionally, bEVs were orally administered weekly for six weeks to high-fat diet-induced obese mice and lean mice. Metabolic phenotype characteristics and EC-dependent vasorelaxation were evaluated. Results: bEV pre-treatment inhibited LPS-induced expression of inflammatory genes, including IL-6 and IL-1β. It also suppressed phospho-NFkB and VCAM-1 expression. bEVs enhanced EC migration, significantly increasing wound closure. Oral administration of bEVs restored impaired EC-dependent vasorelaxation in the mesenteric artery of obese mice, though metabolic parameters remained unchanged. Conclusion: Our findings demonstrate the beneficial effects of bEVs on EC dysfunction, highlighting their potential as novel therapeutics for cardiovascular diseases. Future studies will focus on identifying specific bEV cargos and further evaluating their therapeutic effects on EC dysfunction.

show abstract