miR-125b-5p in adipose derived stem cells exosome alleviates pulmonary microvascular endothelial cells ferroptosis via Keap1/Nrf2/GPX4 in sepsis lung injury
Quick Facts
- Publication title: miR-125b-5p in adipose derived stem cells exosome alleviates pulmonary microvascular endothelial cells ferroptosis via Keap1/Nrf2/GPX4 in sepsis lung injury
- Journal: Redox Biol
- Year: 2023
- DOI: 10.1016/j.redox.2023.102655
- PMID/PMCID: 36913799; PMC10023991
Research overview
This study is meant to explore the protective effect and mechanism of ADSCs exosomes on excessive inflammation PMVECs injury. Collectively, we illustrated a novel potentially therapeutic mechanism that miR-125b-5p in ADSCs exosomes could alleviate the inflammation induced PMVECs ferroptosis in sepsis induced acute lung injury via regulating Keap1/Nrf2/GPX4 expression, hence improve the acute lung injury in sepsis.
Key findings
We successfully isolated ADSCs exosomes, the characteristic of which were confirmed.
ADSCs exosomes reduced excessive inflammatory response induced ROS accumulation and cell injury in PMVECs.
Besides, ADSCs exosomes inhibited excessive inflammatory response induced ferroptosis while upregulated expression of GPX4 in PMVECs.
And further GPX4 inhibition experiments revealed that ADSCs exosomes alleviated inflammatory response induced ferroptosis via upregulating GPX4.
Echo Biotech Role
Echo Biotech contributed cargo loading; the study also used or cited ExoLoad®.
Related platforms: Echosome®, Research Reagents & Tools
Related services and capabilities: Small RNA / Cargo Loading, Research Reagent / Product Supply
Related products or reagents: ExoLoad® Nucleic Acid Loading Kit
References
Original publication: miR-125b-5p in adipose derived stem cells exosome alleviates pulmonary microvascular endothelial cells ferroptosis via Keap1/Nrf2/GPX4 in sepsis lung injury Redox Biol. 2023. DOI: 10.1016/j.redox.2023.102655. PMID/PMCID: 36913799; PMC10023991.