Mesenchymal Stem Cell-Conditioned Media Modulate HUVEC Response to H 2 O 2 : Impact on Gene Expression and Potential for Atherosclerosis Intervention
We studied the potential of human bone marrow-derived mesenchymal stem cell conditioned media (hBMSC CM) in protecting endothelial cell properties (viability, proliferation, and migrations) from the deleterious effects produced by the inflammatory environment of H O . Additionally, we investigated t...
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Veröffentlicht in: | BioMed research international 2024, Vol.2024 (1), p.7726493 |
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Sprache: | eng |
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Zusammenfassung: | We studied the potential of human bone marrow-derived mesenchymal stem cell conditioned media (hBMSC CM) in protecting endothelial cell properties (viability, proliferation, and migrations) from the deleterious effects produced by the inflammatory environment of H
O
. Additionally, we investigated their impact on the endothelial cells' gene expression of some inflammatory-related genes, namely, TGF-
1, FOS, ATF3, RAF-1, and SMAD3.
Human umbilical vein endothelial cells (HUVECs) were cultured individually under three conditions: alone, with varying concentrations of H
O
, or with varying concentrations of H
O
and hBMSC CM. HUVEC adhesion, proliferation, and migration were evaluated using the xCELLigence system. The HUVECs' gene expressions were evaluated by real-time polymerase chain reaction (RT-PCR).
Generally, we observed enhanced HUVEC viability, proliferation, and migration when cultured in media supplemented with H
O
and hBMSC CM. Furthermore, the CM modulated the expressions of the studied inflammatory-related genes in HUVECs, promoting a more robust cellular response.
This study has illuminated the protective role of hBMSC CM in mitigating the damaging effects of H
O
on endothelial cell function. Our data demonstrate that hBMSC CM enhances the viability, proliferation, and migration of HUVECs even under oxidative stress conditions. Additionally, the conditioned medium was found to modulate the gene expression of pivotal markers related to inflammation, suggesting a favorable influence on cellular response mechanisms. |
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ISSN: | 2314-6133 2314-6141 |
DOI: | 10.1155/2024/7726493 |