scholarly journals Mesenchymal stem cells and cell-derived extracellular vesicles protect hippocampal neurons from oxidative stress and synapse damage induced by amyloid-β oligomers

2017 ◽  
Vol 293 (6) ◽  
pp. 1957-1975 ◽  
Author(s):  
Mariana A. de Godoy ◽  
Leonardo M. Saraiva ◽  
Luiza R. P. de Carvalho ◽  
Andreia Vasconcelos-dos-Santos ◽  
Hellen J. V. Beiral ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Hippocampal Neurons ◽  
Amyloid Β

scholarly journals Extracellular vesicles derived from human Wharton’s jelly mesenchymal stem cells protect hippocampal neurons from oxidative stress and synapse damage induced by amyloid-β oligomers

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Victor Bodart-Santos ◽  
Luiza R. P. de Carvalho ◽  
Mariana A. de Godoy ◽  
André F. Batista ◽  
Leonardo M. Saraiva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Wharton’S Jelly ◽  
Wharton's Jelly

Abstract Background Mesenchymal stem cells (MSCs) have been explored as promising tools for treatment of several neurological and neurodegenerative diseases. MSCs release abundant extracellular vesicles (EVs) containing a variety of biomolecules, including mRNAs, miRNAs, and proteins. We hypothesized that EVs derived from human Wharton’s jelly would act as mediators of the communication between hMSCs and neurons and could protect hippocampal neurons from damage induced by Alzheimer’s disease-linked amyloid beta oligomers (AβOs). Methods We isolated and characterized EVs released by human Wharton’s jelly mesenchymal stem cells (hMSC-EVs). The neuroprotective action of hMSC-EVs was investigated in primary hippocampal cultures exposed to AβOs. Results hMSC-EVs were internalized by hippocampal cells in culture, and this was enhanced in the presence of AβOs in the medium. hMSC-EVs protected hippocampal neurons from oxidative stress and synapse damage induced by AβOs. Neuroprotection by hMSC-EVs was mediated by catalase and was abolished in the presence of the catalase inhibitor, aminotriazole. Conclusions hMSC-EVs protected hippocampal neurons from damage induced by AβOs, and this was related to the transfer of enzymatically active catalase contained in EVs. Results suggest that hMSC-EVs should be further explored as a cell-free therapeutic approach to prevent neuronal damage in Alzheimer’s disease.

scholarly journals Alteration of payload in extracellular vesicles by crosstalk with mesenchymal stem cells from different origin

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Dong Jun Park ◽  
Jeong-Eun Park ◽  
Tae Hoon Kong ◽  
Young Joon Seo
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Cell Damage ◽  
Recipient Cell ◽  
Amyloid Β ◽  
Inflammatory Factors ◽  
Target Disease ◽  
Human Middle Ear ◽  
Different Origins

Abstract Background The application of extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) requires customized materials to target disease or cell damage. We hypothesized that EVs exert different inflammatory effects on one recipient cell, although stem cells of different origins in humans have similar payloads. Results Here, the payload of EVs released by crosstalk between MSCs and human middle ear epithelial cells (HMEECs) extracted from adipose tissue, bone marrow and tonsils significantly increased the level of anti-inflammatory factors. EVs derived from the co-culture medium decreased TNF-α, COX-2, IL-1β, and IL-6 levels to approximately zero within 3 h in HMEECs. Expression of miR-638 and amyloid-β A4 precursor protein-binding family A member 2 was analyzed using microarrays and gene ontology analysis, respectively. Conclusions In conclusion, stem cells of different origins have different payloads through crosstalk with recipient-specific cells. Inducing specific factors in EVs by co-culture with MSCs could be valuable in regenerative medicine. Graphical abstract

scholarly journals Extracellular vesicles produced by bone marrow mesenchymal stem cells attenuate renal fibrosis, in part by inhibiting the RhoA/ROCK pathway, in a UUO rat model

2020 ◽  
Author(s):  
Zhengzhou Shi ◽  
Qi Wang ◽  
Youbo Zhang ◽  
Dapeng Jiang
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Rat Model ◽  
Renal Fibrosis ◽  
Marrow Mesenchymal Stem Cells ◽  
Hk2 Cells ◽  
Tgf Β1

Abstract Background: Renal interstitial fibrosis is a critical symptom of chronic kidney disease that is associated with high incidence. Extracellular vesicles produced by bone marrow mesenchymal stem cells (BMSC-EVs) can play important roles in the repair of injured tissues. Though numerous studies have reported the effect of EVs on renal fibrosis, the underlying mechanisms remain unclear. We hypothesized that BMSC-EVs containing milk fat globule–epidermal growth factor–factor 8 (MFG-E8) could attenuate renal fibrosis by inhibiting the RhoA/ROCK pathway. Methods: We investigated whether BMSC-EVs have antifibrotic effects in a rat model of renal fibrosis, in which rats were subjected to unilateral ureteral obstruction (UUO), as well as in cultured HK2 cells. Extracellular vesicles from BMSCs were collected and co-cultured with HK2 cells during transforming growth factor-β1 (TGF-β1) treatment. HK2 cells co-cultured with TGF-β1 were also treated with the ROCK inhibitor, Y-27632. Results: Compared with the Sham group, UUO rats displayed fibrotic abnormalities, accompanied by an increased expression of α-smooth muscle actin and Fibronectin and reduced expression of E-cadherin. These molecular and pathological changes suggested increased inflammation in damaged kidneys. Oxidative stress, as evidenced by decreased levels of SOD1 and Catalase, was also observed in UUO kidneys. Additionally, activation of cleaved caspase-3 and PARP1 and increased apoptosis in the proximal tubules confirmed tubular cell apoptosis in the UUO group. All of these phenotypes exhibited by UUO rats were suppressed by treatment with BMSC-EVs. However, the protective effect of BMSC-EVs was completely abolished by the inhibition of MFG-E8. Consistent with the in vivo results, treatment with BMSC-EVs reduced inflammation, oxidative stress, apoptosis, and fibrosis in HK-2 cells stimulated with TGF-β1 in vitro. Interestingly, treatment with Y-27632 protected HK-2 cells against inflammation and fibrosis, although oxidative stress and apoptosis were unchanged. Conclusions: Our results show that BMSC-EVs containing MFG-E8 attenuate renal fibrosis in a rat model of renal fibrosis, partly through RhoA/ROCK pathway inhibition.

Mesenchymal stem cells enhances the viability of primary culture of rat hippocampal neurons under oxidative stress

2010 ◽  
Vol 34 (8) ◽  
pp. S40-S40
Author(s):  
Yang Liu ◽  
Ting Ting Sun ◽  
Xiao Hua Jiang ◽  
Ting Yu Li ◽  
Hsiao Chang Chan
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Primary Culture ◽  
Hippocampal Neurons

scholarly journals Transplantation of Mesenchymal Stem Cells Improves Amyloid-β Pathology by Modifying Microglial Function and Suppressing Oxidative Stress

2019 ◽  
Vol 72 (3) ◽  
pp. 867-884 ◽  
Author(s):  
Kazuki Yokokawa ◽  
Naotoshi Iwahara ◽  
Shin Hisahara ◽  
Miho C. Emoto ◽  
Taro Saito ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Amyloid Β
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