ArticleCell & bioscience2018
Transplantation of endothelial progenitor cells attenuated paraquat-induced acute lung injury via miR-141-3p-Notch-Nrf2 axis.
Article in Cell & bioscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Diabetic neuropathy: cutting-edge research and future directions.Signal transduction and targeted therapy · 2025Review
- miR-141-3p attenuates inflammation and oxidative stress-induced pulmonary fibrosis in ARDS via the Keap1/Nrf2/ARE signaling pathway.Immunologic research · 2024Article
- E2F1 regulates miR-215-5p to aggravate paraquat-induced pulmonary fibrosis via repressing BMPR2 expression.Toxicology research · 2022Article
- Exosome-derived circTRPS1 promotes malignant phenotype and CD8+ T cell exhaustion in bladder cancer microenvironments.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Protective effect of endothelial progenitor cell-derived exosomal microRNA-382-3p on sepsis-induced organ damage and immune suppression in mice.American journal of translational research · 2022Article
- Anthrahydroquinone-2-6-disulfonate is a novel, powerful antidote for paraquat poisoning.Scientific reports · 2021Article
- Role of Nrf2 and Its Activators in Cardiocerebral Vascular Disease.Oxidative medicine and cellular longevity · 2020Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParaquat (PQ) presents with high toxicity for humans and animals, and the lungs become the main target organ by the poisoning of PQ leading to acute lung injury. Endothelial progenitor cells (EPCs) were proved to have the repair function on acute lung injury (ALI). We aimed to invatigate the underlying mechanism of EPCs in PQ-induced ALI involving miR-141-3p.
methodsEndothelial progenitor cells were isolated from peripheral blood of C57BL/6J mice and identified by flow cytometry. Lung wet-to-dry (W/D) weight ratios, lung injury score and the number of total leukocyte and the number of neutrophils in BALF were used to analyze the degree of lung injury. The transfection was performed with Lipofectamine 2000. The levels of miRNA and mRNA were determined by qRT-PCR, and the protein levels were detected by Western blot assay.
resultsEndothelial progenitor cells alleviated lung wet-to-dry (W/D) weight ratios, lung injury score and the number of total leukocyte and the number of neutrophils in BALF in PQ-induced ALI mice. EPCs inhibited miR-141-3p expression, and enhanced the levels of Notch-Nrf2 axis in PQ-induced ALI mice. MiR-141-3p knockdown reversed the PQ induced-inhibition on Notch-1 and Hesr1 expression. MiR-141-3p over-expression could inhibit the expression of Notch-1 pathway significantly in the pulmonary epithelial cell line MLE-12. Both miR-141-3p over-expression and si-Notch-1 abolished the protection effect of EPCs on lung injury induced by PQ in vivo.
conclusionsEndothelial progenitor cells could provide therapeutic effect on PQ-induced ALI via miR-141-3p-Notch-Nrf2 Axis.
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