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Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli

dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorLUIS ANGEL MACIEL BARONes_MX
dc.creatorSANDRA LIZBETH MORALES ROSALESes_MX
dc.creatorANGELICA ALEJANDRA AQUINO CRUZes_MX
dc.creatorFRANCISCO TRIANA MARTINEZes_MX
dc.creatorSONIA GALVAN ARZATEes_MX
dc.creatorARMANDO LUNA LOPEZes_MX
dc.creatorVIRIDIANA YAZMIN GONZALEZ PUERTOSes_MX
dc.creatorNORMA EDITH LOPEZ DIAZ GUERREROes_MX
dc.creatorClaudio Torreses_MX
dc.creatorMINA KONIGSBERG FAINSTEINes_MX
dc.date2016
dc.date.accessioned2021-12-02T20:20:44Z
dc.date.available2021-12-02T20:20:44Z
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17324
dc.descriptionCellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as an important feature during tumor suppression mechanisms and a contributor to aging. Senescent cells have an altered secretion pattern called Senescence-Associated Secretory Phenotype (SASP) that comprises a complex mix of factors including cytokines, growth factors, chemokines, and matrix metalloproteinases. SASP has been related with local inflammation that leads to cellular transformation and neurodegenerative diseases. Various pathways for senescence induction have been proposed; the most studied is replicative senescence due to telomere attrition called replicative senescence (RS). However, senescence can be prematurely achieved when cells are exposed to diverse stimuli such as oxidative stress (stress-induced premature senescence, SIPS) or proteasome inhibition (proteasome inhibition-induced premature senescence, PIIPS). SASP has been characterized in RS and SIPS but not in PIIPS. Hence, our aim was to determine SASP components in primary lung fibroblasts obtained from CD-1 mice induced to senescence by PIIPS and compare them to RS and SIPS. Our results showed important variations in the 62 cytokines analyzed, while SIPS and RS showed an increase in the secretion of most cytokines, and in PIIPS only 13 were incremented. Variations in glutathione-redox balance were also observed in SIPS and RS, and not in PIIPS. All senescence types SASP displayed a pro-inflammatory profile and increased proliferation in L929 mice fibroblasts exposed to SASP. However, the behavior observed was not exactly the same, suggesting that the senescence induction pathway might encompass dissimilar responses in adjacent cells and promote different outcomes.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherSpringeres_MX
dc.relationhttps://link.springer.com/article/10.1007/s11357-016-9886-1es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceAge (2509-2723) Vol. 38 (2016)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectBiología celulares_MX
dc.subjectEnvejecimientoes_MX
dc.subjectAginges_MX
dc.subjectSenectudes_MX
dc.subjectSenescencees_MX
dc.subjectSenescence-Associated Secretory Phenotype (SASP)es_MX
dc.subjectFenotipo secretor asociado a la senescenciaes_MX
dc.subjectEstrés oxidativoes_MX
dc.subjectOxidative stresses_MX
dc.titleSenescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimulies_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
dc.creator.idMABL870228HDFCRS00es_MX
dc.creator.idMORS910315MDFRSN07es_MX
dc.creator.idAUCA900712MDFQRN07es_MX
dc.creator.idTIMF860407HOCRRR01es_MX
dc.creator.idGAAS650725MDFLRN03es_MX
dc.creator.idLULA690630HDFNPR02es_MX
dc.creator.idGOPV820119MDFNRR03es_MX
dc.creator.idLODN680314MDFPZR02es_MX
dc.creator.id0000-0002-3727-7391es_MX
dc.creator.idKOFM650625MDFNNN02es_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercvues_MX
dc.creator.nameIdentifiercurpes_MX


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