<abstract xmlns="http://www.w3.org/1999/xhtml">

<bold>Background</bold>: Diabetes is a common chronic disease which has caused a great burden on families and society. The treatment of diabetes has always been a hotspot. This study aimed to explore the effect and mechanism of miR-30d-5pon inflammation of high glucose-impaired human keloid fibroblasts (HKF).
<bold>Methods</bold>: Differently-expressed miRNAs were predicted by bioinformatics methods. Exosomes were observed by transmission electron microscope. Exosome particle sizes were measured by NanoSight. Western Blot was used to detect the expression of CD81, CD63, CD9, and Calnexin. QRT-PCR was used to detect the expression of miR-30d-5p, IL-1β, TNF-α, VEGF, FGF21, NRF2, and HO-1. The levels of IL-1β, TNF-α, IL-6, IL-10, and TGF-β were determined by ELISA. Cell apoptosis and CD86, CD206 positive cells were detected by flow cytometry.
<bold>Results</bold>: Tori formula could promote the secretion of endothelial progenitor cell (EPCs) exosomes. EPCs exosomes and miR-30d-5p could stimulate the proliferation of HKF impaired by high glucose and the expression of IL-10 and TGF-β. MiR-30d-5p inhibited the proliferation of M1 macrophages and the expression of IL-1β and TNF-α. It could also promote the proliferation of M2 macrophages and the expression of CCL17 and CCL22. Moreover, miR-30d-5p stimulated the expression of VEGF, FGF21, NRF2, and HO-1, as well as suppressed the expression of IL-1β, TNF-α, and IL-6. MiR-30d-5p also restrained the apoptosis of impaired HKF. <bold>Conclusion</bold>: This study confirmed that miR-30d-5p could promote the M1/M2 polarization and inhibit the inflammatory response of impaired HKF, which provided a certain idea and direction for treating diabetes.
</abstract>

Background: Diabetes is a common chronic disease which has caused a great burden on families and society. The treatment of diabetes has always been a hotspot. This study aimed to explore the effect and mechanism of miR-30d-5pon inflammation of high glucose-impaired human keloid fibroblasts (HKF).
Methods: Differently-expressed miRNAs were predicted by bioinformatics methods. Exosomes were observed by transmission electron microscope. Exosome particle sizes were measured by NanoSight. Western Blot was used to detect the expression of CD81, CD63, CD9, and Calnexin. QRT-PCR was used to detect the expression of miR-30d-5p, IL-1β, TNF-α, VEGF, FGF21, NRF2, and HO-1. The levels of IL-1β, TNF-α, IL-6, IL-10, and TGF-β were determined by ELISA. Cell apoptosis and CD86, CD206 positive cells were detected by flow cytometry.
Results: Tori formula could promote the secretion of endothelial progenitor cell (EPCs) exosomes. EPCs exosomes and miR-30d-5p could stimulate the proliferation of HKF impaired by high glucose and the expression of IL-10 and TGF-β. MiR-30d-5p inhibited the proliferation of M1 macrophages and the expression of IL-1β and TNF-α. It could also promote the proliferation of M2 macrophages and the expression of CCL17 and CCL22. Moreover, miR-30d-5p stimulated the expression of VEGF, FGF21, NRF2, and HO-1, as well as suppressed the expression of IL-1β, TNF-α, and IL-6. MiR-30d-5p also restrained the apoptosis of impaired HKF. Conclusion: This study confirmed that miR-30d-5p could promote the M1/M2 polarization and inhibit the inflammatory response of impaired HKF, which provided a certain idea and direction for treating diabetes.

Endothelial progenitor cell (EPCs)-derived exosomal miR-30d-5p inhibits the inflammatory response of high glucose-impaired fibroblasts by affecting the M1/M2 polarization of macrophages

the First Affiliated Hospital of Hunan University of Chinese Medicine

Department of plastic surgery, Xiangya Third Hospital

Hunan Brain Hospital (Clinical Medical School of Hunan University of Chinese Medicine)

Revista Romana de Medicina de Laborator

This work is licensed under the Creative Commons Attribution 4.0 International License.

Background: Diabetes is a common chronic disease which has caused a great burden on families and society. The treatment of diabetes has always been a hotspot....

Endothelial progenitor cell (EPCs)-derived exosomal miR-30d-5p inhibits the inflammatory response of high glucose-impaired fibroblasts by affecting the M1/M2 polarization of macrophages

Pubblicato online: 20 ott 2022

Pagine: 435 - 451

Ricevuto: 12 mag 2022

Accettato: 25 giu 2022

DOI: https://doi.org/10.2478/rrlm-2022-0032

Parole chiave
diabetes mellitus, miR-30d-5p, high-glucose impaired HKF, EPCs exosomes

© 2022 Wu Xiong et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Endothelial progenitor cell (EPCs)-derived exosomal miR-30d-5p inhibits the inflammatory response of high glucose-impaired fibroblasts by affecting the M1/M2 polarization of macrophages

Pubblicato online: 20 ott 2022

Pagine: 435 - 451

Ricevuto: 12 mag 2022

Accettato: 25 giu 2022

DOI: https://doi.org/10.2478/rrlm-2022-0032

Parole chiavediabetes mellitus, miR-30d-5p, high-glucose impaired HKF, EPCs exosomes

© 2022 Wu Xiong et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Parole chiave
diabetes mellitus, miR-30d-5p, high-glucose impaired HKF, EPCs exosomes