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

ISSN online: 2284-5623

ISSN-L: 1841-6624

Rejection rate (2020): 75%

Română English


Journal Metrics

Impact Factor 0.5
Five Year Impact Factor 0.5
JCI 0.12


Advanced search


Top 10 downloaded articles
- May 2024 -
 
A comprehensive review of Prof... 26
Effect of Systemic Inflammator... 15
The role of nitro oxidative fa... 14
Diagnostic value of stress myo... 14
Evaluation of routine laborato... 13
Romanian Review of Laboratory ... 12
Correlations of expressions of... 12
Monitoring the sensitivity of ... 11
Evaluation of cytotoxicity and... 10
Understanding the key differen... 8

Log in

Concept, Design & Programming
Dr. Adrian Man

   
 
Nr. 30(4)/2022 DOI:10.2478/rrlm-2022-0032
XML
TXT

Research article

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

Wu Xiong, Mei-xin Tan, Zi-lin Chen, Yu Liu, Yang Liu, Xiao-ling Zou, Xiao-qin Wang, Ya Yang, Pei Tan, Xi Zhang

Correspondence should be addressed to: Xi Zhang

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.

Keywords: diabetes mellitus, miR-30d-5p, high-glucose impaired HKF, EPCs exosomes

Received: 12.5.2022
Accepted: 25.6.2022
Published: 16.8.2022

 
  PDF Download full text PDF
(4471 KB)
     
 
How to cite
Xiong W, Tan Mx, Chen Zl, Liu Y, Liu Y, Zou Xl, et al. Endothelial progenitor cell (EPCs)-derived exosomal miR-30d-5p inhibits the inflammatory response of high glucose-impaired fibroblasts by affecting the polarization of M1/M2 macrophage. Rev Romana Med Lab. 2022;30(4):435-51. DOI:10.2478/rrlm-2022-0032