Copyright (c) 2023 Jinye Lu, Beibei Gu, Xinlu Han, Yinnan Feng
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Mammary epithelial cell-derived exosomal miR-155-inhibitor played a key role in the treatment of mastitis via down-regulation of TLRs/NF-κB signaling pathway to inhibit inflammatory response
Corresponding Author(s) : Jinye Lu
Cellular and Molecular Biology,
Vol. 69 No. 15: New discoveries in inflammatory factors
Abstract
Mastitis is a common disorder in women capable of altering the normal physiological function of the mammary gland. It has been reported that mammary epithelial cells (MECs) could be involved in treating mastitis by regulating the inflammatory response and miR-155 might participate in this process. However, the effects of MECs-derived exosomal miR-155-inhibitor in treating mastitis and the regarding mechanism are still unknown. In our study, mouse mammary epithelial cells (HC11) were applied to study the role of MECs-derived exosomal miR-155-inhibitor in the treatment of mastitis and explore the mechanism. Results in our study showed that specific markers including CD63 and Apo-A1 were expressed in blank exosomes and exosomes containing miR-155-inhibitor isolated from transfected HC11 cells. Results of immunofluorescence showed that the blank exosomes and exosomes (containing miR-155-inhibitor) labeled with PKH26 were absorbed in HC11 cells. The level of miR-155 was decreased obviously in Engineered exosomes with miR-155-inhibitor and HC11 cells Transfected with exosome containing miR-155-inhibitor. The level of miR-155 was increased and cell apoptosis was promoted obviously in HC11 cells induced by LPS, however, they were decreased obviously after transfecting with an exosome containing miR-155-inhibitor. The level of TLR2, TLR4, TLR6, NF-κB, TNF-α, and IL-1β was increased obviously in LPS-induced HC11 cells, however, they were decreased obviously after transfecting with an exosome containing miR-155-inhibitor. The change in IL-10 level is opposite to the above genes. Taken together, exosomal miR-155-inhibitor could decrease the apoptosis of MECs and inhibit the inflammatory response to treat mastitis by down-regulation in the TLRs/NF-κB signaling pathway, which might be a new therapeutic target for mastitis.
Keywords
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX
