RGD Reference Report - Extracellular vesicles derived from EphB2-overexpressing bone marrow mesenchymal stem cells ameliorate DSS-induced colitis by modulating immune balance. - Rat Genome Database

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Extracellular vesicles derived from EphB2-overexpressing bone marrow mesenchymal stem cells ameliorate DSS-induced colitis by modulating immune balance.

Authors: Yu, Ting  Chu, Si  Liu, Xingxing  Li, Junyi  Chen, Qianyun  Xu, Meng  Wu, Hui  Li, Mingyue  Dong, Yalan  Zhu, Feng  Zhou, Haifeng  Hu, Desheng  Fan, Heng 
Citation: Yu T, etal., Stem Cell Res Ther. 2021 Mar 15;12(1):181. doi: 10.1186/s13287-021-02232-w.
RGD ID: 127285641
Pubmed: PMID:33722292   (View Abstract at PubMed)
PMCID: PMC7962309   (View Article at PubMed Central)
DOI: DOI:10.1186/s13287-021-02232-w   (Journal Full-text)


BACKGROUND: The bone marrow mesenchymal stem cell (BMSCs)-derived extracellular vesicles (EVs) open up a new avenue for ulcerative colitis (UC) treatment recently, but they are not selectively enriched in targeted tissues. EphB2, a cell-to-cell signaling receptor, is identified as a regulator for inflammatory response, immune homeostasis and cell migration. In this study, we investigated the therapeutic potential and underlying mechanism for EphB2 over-expressing BMSCs derived EVs (EphB2-EVs) in the treatment of UC.
METHODS: BMSCs and EVs were obtained and characterized by a series of experiments. Lentivirus vector encoding EphB2 was transfected into BMSCs and verified by qRT-PCR. We analyzed the EphB2-EVs ability of colonic targeting in a DSS-induced colitis model by using confocal microscope and WB. The protective effect of EphB2-EVs in vivo was systematically evaluated by using a series of function experiments.
RESULTS: We successfully constructed EphB2-overexpressing BMSCs derived EVs (EphB2-EVs). Overexpression of EphB2 significantly enhanced the homing of EVs to the damaged colon. In addition, EphB2-EVs were effective to attenuate inflammation in intestinal mucosa and restore the damaged colon tissue by inhibiting the release of proinflammatory cytokines and upregulating the anti-inflammatory mediators. EphB2-EVs effectively reduced the oxidative stress and repaired the intestinal mucosal barrier in the UC rats. Moreover, EphB2-EVs demonstrated a robust immunomodulatory effect to restore immune homeostasis via modulating Th17/Treg balance and restraining STAT3 activation.
CONCLUSIONS: Our results suggest that EphB2-EVs have high colonic targeting ability and could mitigate DSS-induced colitis via maintaining colonic immune homeostasis. These findings provide an effective therapeutic strategy for UC treatment in clinic.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
EPHB2Humanulcerative colitis amelioratesISOEphb2 (Rattus norvegicus) RGD 
Ephb2Ratulcerative colitis amelioratesIDA  RGD 
Ephb2Mouseulcerative colitis amelioratesISOEphb2 (Rattus norvegicus) RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  

Objects Annotated

Genes (Rattus norvegicus)
Ephb2  (Eph receptor B2)

Genes (Mus musculus)
Ephb2  (Eph receptor B2)

Genes (Homo sapiens)
EPHB2  (EPH receptor B2)


Additional Information