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dc.contributor.authorDemircan, Turan
dc.contributor.authorHacıbektaşoğlu, Harbiye
dc.contributor.authorSibai, Mustafa
dc.contributor.authorCana Fesçioğlu, Ece
dc.contributor.authorAltuntaş, Ebru
dc.contributor.authorÖztürk, Gürkan
dc.contributor.authorSüzek, Barış Ethem
dc.date.accessioned2020-07-07T16:31:20Z
dc.date.available2020-07-07T16:31:20Z
dc.date.issued2020en_US
dc.identifier.citationDemircan, T., Hacıbektaşoğlu, H., Sibai, M., Cana Fesçioğlu, E., Altuntaş, E., Öztürk, G. ... Süzek, B. E. (2020). Preclinical molecular signatures of spinal cord functional restoration: Optimizing the metamorphic axolotl (ambystoma mexicanum) model in regenerative medicine. OMICS: A Journal of Integrative Biology, 24(6), 370-378. https://dx.doi.org/10.1089/omi.2020.0024en_US
dc.identifier.issn1536-2310
dc.identifier.issn1557-8100
dc.identifier.urihttps://dx.doi.org/10.1089/omi.2020.0024
dc.identifier.urihttps://hdl.handle.net/20.500.12511/5420
dc.description.abstractRegenerative medicine offers hope for patients with diseases of the central and peripheral nervous system. Urodele amphibians such as axolotl display an exceptional regenerative capacity and are considered as essential preclinical model organisms in neurology and regenerative medicine research. Earlier studies have suggested that the limb regeneration ability of this salamander notably decreases with induction of metamorphosis by thyroid hormones. Metamorphic axolotl requires further validation as a negative control in preclinical regenerative medicine research, not to mention the study of molecular substrates of its regenerative abilities. In this study, we report new observations on the effect of experimentally induced metamorphosis on spinal cord regeneration in axolotl. Surprisingly, we found that metamorphic animals were successful to functionally restore the spinal cord after an experimentally induced injury. To discern the molecular signatures of spinal cord regeneration, we performed transcriptomics analyses at 1- and 7-days postinjury (dpi) for both spinal cord injury (SCI)-induced (experimental) and laminectomy (sham) groups. We observed 119 and 989 differentially expressed genes at 1- and 7-dpi, respectively, while the corresponding mouse orthologous genes were enriched in junction-, immune system-, and extracellular matrix-related pathways. Taken together, our findings challenge the prior notions of limited regenerative ability of metamorphic axolotl which exhibited successful spinal cord regeneration in our experience. Moreover, we report on molecular signatures that can potentially explain the mechanistic substrates of the regenerative capacity of the metamorphic axolotl. To the best of our knowledge, this is the first report on molecular responses to SCI and functional restoration in metamorphic axolotls. These new findings advance our understanding of spinal cord regeneration, and may thus help optimize the future use of axolotl as a preclinical model in regenerative medicine and integrative biology fields.en_US
dc.language.isoengen_US
dc.publisherMary Ann Lieberten_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectRegenerative Medicineen_US
dc.subjectNeuroscienceen_US
dc.subjectSpinal Cord Injuryen_US
dc.subjectMetamorphic Axolotlen_US
dc.subjectBiomarkersen_US
dc.subjectPreclinical Modelsen_US
dc.titlePreclinical molecular signatures of spinal cord functional restoration: Optimizing the metamorphic axolotl (ambystoma mexicanum) model in regenerative medicineen_US
dc.typearticleen_US
dc.relation.journalOMICS: A Journal of Integrative Biologyen_US
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)en_US
dc.departmentİstanbul Medipol Üniversitesi, Uluslararası Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalıen_US
dc.authorid0000-0003-0352-1947en_US
dc.identifier.volume24en_US
dc.identifier.issue6en_US
dc.identifier.startpage370en_US
dc.identifier.endpage378en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1089/omi.2020.0024en_US


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