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Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells
dc.contributor.author | Mato-Basalo, Rocío | |
dc.contributor.author | Morente-López, Miriam | |
dc.contributor.author | Arntz, O.J. | |
dc.contributor.author | Van de Loo, F.J. | |
dc.contributor.author | Fafián Labora, Juan Antonio | |
dc.contributor.author | Arufe, M.C. | |
dc.date.accessioned | 2021-04-05T19:35:19Z | |
dc.date.available | 2021-04-05T19:35:19Z | |
dc.date.issued | 2021-03-25 | |
dc.identifier.citation | Mato-Basalo R, Morente-López M, Arntz OJ, van de Loo FAJ, Fafián-Labora J, Arufe MC. Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells. Int J Mol Sci. 2021 Mar 25;22(7):3367. | es_ES |
dc.identifier.issn | 1661-6596 | |
dc.identifier.uri | http://hdl.handle.net/2183/27661 | |
dc.description.abstract | [Abstract] Mesenchymal stem cells have an important potential in the treatment of age-related diseases. In the last years, small extracellular vesicles derived from these stem cells have been proposed as cell-free therapies. Cellular senescence and proinflammatory activation are involved in the loss of therapeutic capacity and in the phenomenon called inflamm-aging. The regulators of these two biological processes in mesenchymal stem cells are not well-known. In this study, we found that p65 is activated during cellular senescence and inflammatory activation in human umbilical cord-derived mesenchymal stem cell. To demonstrate the central role of p65 in these two processes, we used smallmolecular inhibitors of p65, such as JSH-23, MG-132 and curcumin. We found that the inhibition of p65 prevents the cellular senescence phenotype in human umbilical cord-derived mesenchymal stem cells. Besides, p65 inhibition produced the inactivation of proinflammatory molecules as components of a senescence-associated secretory phenotype (SASP) (interleukin-6 and interleukin-8 (IL-6 and IL-8)). Additionally, we found that the inhibition of p65 prevents the transmission of paracrine senescence between mesenchymal stem cells and the proinflammatory message through small extracellular vesicles. Our work highlights the important role of p65 and its inhibition to restore the loss of functionality of small extracellular vesicles from senescent mesenchymal stem cells and their inflamm-aging signature. | es_ES |
dc.description.sponsorship | This work was funded by the Spanish National Health Institute Carlos III (PI20/00497) awarded to M.C.A. J.F.L was funded by the Xunta de Galicia Fellowship (ED481B 2017/117). | es_ES |
dc.description.sponsorship | Xunta de Galicia; ED481B 2017/117 | es_ES |
dc.description.sponsorship | info:eu-repo/grantAgreement/ISCIII/Programa Estatal de Generación de Conocimiento y Fortalecimiento del Sistema Español de I+D+I/PI20%2F00497/ES/TERAPIA CELULAR CON MICRO ARN Y VESICULAS EXTRACELULARES PARA EL TRATAMIENTO DE LA INFLAMACION CRONICA EN UN MODELO DE OA. (TERAPIA LIBRE DE CELULAS) | |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.relation.uri | https://doi.org/10.3390/ijms22073367 | es_ES |
dc.rights | Creative Commons Attribution 4.0 International License (CC-BY 4.0) | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | Mesenchymal stem cells | es_ES |
dc.subject | Inflamm-aging | es_ES |
dc.subject | Cellular senescence | es_ES |
dc.subject | SASP | es_ES |
dc.subject | sEV | es_ES |
dc.title | Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.rights.access | info:eu-repo/semantics/openAccess | es_ES |
UDC.journalTitle | International Journal of Molecular Sciences | es_ES |
UDC.volume | 22 | es_ES |
UDC.issue | 7 | es_ES |
UDC.startPage | 3367 | es_ES |
dc.identifier.doi | 10.3390/ijms22073367 |
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