Mesenchymal stem cell secretome protects against oxidative stress-induced ocular blast visual pathologies

2022 ◽  
pp. 108930
Author(s):  
Kumar Abhiram Jha ◽  
Pratheepa Kumari Rasiah ◽  
Jordy Gentry ◽  
Nobel A. Del Mar ◽  
Ravi Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Mesenchymal Stem Cell

Intranasal delivery of mesenchymal stem cell-derived exosomes reduces oxidative stress and markedly inhibits ethanol consumption and post-deprivation relapse drinking.

2018 ◽  
Vol 24 (5) ◽  
pp. 994-1007 ◽  
Author(s):  
Fernando Ezquer ◽  
María Elena Quintanilla ◽  
Paola Morales ◽  
Daniela Santapau ◽  
Marcelo Ezquer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Ethanol Consumption ◽  
Intranasal Delivery

scholarly journals Mesenchymal stem cell‐derived exosomes ameliorate erection by reducing oxidative stress damage of corpus cavernosum in a rat model of artery injury

2019 ◽  
Vol 23 (11) ◽  
pp. 7462-7473 ◽  
Author(s):  
Yangzhou Liu ◽  
Shankun Zhao ◽  
Lianmin Luo ◽  
Jiamin Wang ◽  
Zhiguo Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Rat Model ◽  
Corpus Cavernosum ◽  
Artery Injury ◽  
Stress Damage

scholarly journals Serum-Mediated Oxidative Stress from Systemic Sclerosis Patients Affects Mesenchymal Stem Cell Function

2017 ◽  
Vol 8 ◽  
Author(s):  
Guillaume Fonteneau ◽  
Claire Bony ◽  
Radjiv Goulabchand ◽  
Alexandre T. J. Maria ◽  
Alain Le Quellec ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Systemic Sclerosis ◽  
Mesenchymal Stem Cell ◽  
Cell Function

Enhanced human mesenchymal stem cell survival under oxidative stress by overexpression of secreted frizzled-related protein 2 gene

2014 ◽  
Vol 94 (2) ◽  
pp. 319-327 ◽  
Author(s):  
Kanjana Pomduk ◽  
Pakpoom Kheolamai ◽  
Yaowalak U-Pratya ◽  
Methichit Wattanapanitch ◽  
Nuttha Klincumhom ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Survival ◽  
Human Mesenchymal Stem Cell ◽  
Related Protein ◽  
Stem Cell Survival

scholarly journals Effects of Mesenchymal Stem Cell-derived Exosomes on Oxidative Stress Responses in Skin Cells

2021 ◽  
Author(s):  
Takaaki Matsuoka ◽  
Keita Takanashi ◽  
Katsuaki Dan ◽  
Kenichi Yamamoto ◽  
Koji Tomobe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cellular Senescence ◽  
Stress Responses ◽  
Dermal Fibroblasts ◽  
Skin Fibroblasts ◽  
Therapeutic Effects ◽  
P53 Expression ◽  
Before And After

Abstract Background: The mechanism by which reactive oxygen species (ROS) produced by oxidative stress promote cellular senescence has been studied in detail. This study aimed to verify the preventive or therapeutic effects of mesenchymal stem cell-derived exosomes (MSC-Ex) on the production of ROS induced by oxidative stress in human skin fibroblasts and clarify the mechanisms that promote cellular senescence.Methods: In a system where H2O2 was applied to skin fibroblasts, we assessed the effects of the application of MSC-Ex before and after oxidative stress and measured the fluctuations in several signaling molecules involved in subsequent intracellular stress responses. Exosomes were isolated from MSCs (MSC-Ex) and normal human dermal fibroblasts (NHDFs, NHDF-Ex) before and after exposure to H2O2. NHDFs were treated with exosomes before and after exposure to H2O2.Results: mRNA expression (aquaporin-1 and aquaporin-3) and hyaluronan secretion associated with skin moisturization were reduced by H2O2 treatment, whereas MSC-Ex reversed these effects. The cellular senescence induced by H2O2 was also reproduced in fibroblasts. Specifically, the downregulation of SIRT1 led to increased acetylated p53 expression over time, which induced the expression of p21, a downstream molecule of p53, and arrested the cell cycle, leading to cell senescence. MSC-Ex enhanced these signal transduction systems. MSC-Ex was also effective at blocking the increase of β-galactosidase activity and accumulation of ROS in cells. This effect was stronger than that of NHDF-Ex.Conclusion: MSC-Ex were found to act defensively against epidermal and cellular senescence induced by oxidative stress.

Mesenchymal stem cell-conditioned media ameliorate diabetic endothelial dysfunction by improving mitochondrial bioenergetics via the Sirt1/AMPK/PGC-1α pathway

2016 ◽  
Vol 130 (23) ◽  
pp. 2181-2198 ◽  
Author(s):  
Yujia Yuan ◽  
Meimei Shi ◽  
Lan Li ◽  
Jingping Liu ◽  
Bo Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Stem Cell ◽  
Protein Kinase ◽  
Endothelial Dysfunction ◽  
Mesenchymal Stem Cell ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Mitochondrial Bioenergetics ◽  
Sirt1 Expression

Vasculopathy is a major complication of diabetes. Impaired mitochondrial bioenergetics and biogenesis due to oxidative stress are a critical causal factor for diabetic endothelial dysfunction. Sirt1, an NAD+-dependent enzyme, is known to play an important protective role through deacetylation of many substrates involved in oxidative phosphorylation and reactive oxygen species generation. Mesenchymal stem cell-conditioned medium (MSC-CM) has emerged as a promising cell-free therapy due to the trophic actions of mesenchymal stem cell (MSC)-secreted molecules. In the present study, we investigated the therapeutic potential of MSC-CMs in diabetic endothelial dysfunction, focusing on the Sirt1 signalling pathway and the relevance to mitochondrial function. We found that high glucose-stimulated MSC-CM attenuated several glucotoxicity-induced processes, oxidative stress and apoptosis of endothelial cells of the human umbilical vein. MSC-CM perfusion in diabetic rats ameliorated compromised aortic vasodilatation and alleviated oxidative stress in aortas. We further demonstrated that these effects were dependent on improved mitochondrial function and up-regulation of Sirt1 expression. MSC-CMs activated the phosphorylation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), leading to direct interaction between Akt and Sirt1, and subsequently enhanced Sirt1 expression. In addition, both MSC-CM and Sirt1 activation could increase the expression of peroxisome proliferator-activated receptor γ co-activator-1α (PGC-1α), as well as increase the mRNA expression of its downstream, mitochondrial, biogenesis-related genes. This indirect regulation was mediated by activation of AMP-activated protein kinase (AMPK). Overall our findings indicated that MSC-CM had protective effects on endothelial cells, with respect to glucotoxicity, by ameliorating mitochondrial dysfunction via the PI3K/Akt/Sirt1 pathway, and Sirt1 potentiated mitochondrial biogenesis, through the Sirt1/AMPK/PGC-1α pathway.

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