Asset Details
Do you wish to reserve the book?
M1 But Not M0 Extracellular Vesicles Induce Polarization of RAW264.7 Macrophages Via the TLR4-NFκB Pathway In Vitro
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
M1 But Not M0 Extracellular Vesicles Induce Polarization of RAW264.7 Macrophages Via the TLR4-NFκB Pathway In Vitro
Do you wish to request the book?
M1 But Not M0 Extracellular Vesicles Induce Polarization of RAW264.7 Macrophages Via the TLR4-NFκB Pathway In Vitro
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
M1 But Not M0 Extracellular Vesicles Induce Polarization of RAW264.7 Macrophages Via the TLR4-NFκB Pathway In Vitro
2020
Overview
AbstractIn response to different stimuli (e.g., infections), naive macrophages polarize into M1 macrophages, which have the potential to secrete numerous pro-inflammatory cytokines and extracellular vesicles (EVs). EVs are important mediators of intercellular communication. Via horizontal transfer, EVs transport various molecules (e.g., proteins, DNA, and RNA) to target cells. This in vitro study elucidated that M1-EVs from macrophages induced by interferon-γ (IFN-γ) and lipopolysaccharide (LPS) 24 h (M1), but not M0-EVs from untreated macrophages (M0), shifted M0 into M1 phenotype via activating the nuclear factor-κB pathway. The characteristics of these EVs were assessed by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and a western blot assay. RAW 264.7 cells were incubated with M1-EVs (experimental group) or PBS (sham group) or M0-EVs (control group) for 24 h. The viability, change of shape, and phenotype differentiation of the macrophages were identified by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and immunofluorescence staining. The TLR4-NFκB pathway of RAW264.7 macrophages was assessed by a western blot assay. M1-EVs but not M0-EVs were incorporated by the RAW264.7 cells and directly induced polarization of RAW264.7 macrophages to M1 macrophages. This polarization was demonstrated by significant upregulation of the M1 macrophage marker CD86 in the experimental group (49.93 ± 5.0%) as compared with that in the control and sham groups (1.22% and 1.46%, respectively) and significant upregulation of iNOS in the experimental group (75 ± 5.0%) as compared with that in the control and sham groups (0%). Furthermore, cell viability was higher (1.3 times) in the experimental group as compared with that in both the sham and control groups. The regulatory mechanism of M1-EVs on RAW 264.7 macrophages polarization and activation was triggered by the activation of the TLR4-NFκB signaling pathway. Based on our observations, we conclude that M1-EVs play an important role in the M1 macrophage auto-polarizing loop. These data clearly demonstrate an important role for macrophage-derived EVs in cellular differentiation. Further studies are needed to elucidate the potential of these EVs in the modulation of inflammatory stimuli.
Publisher
Springer Nature B.V
Subject
