Characterization of mesenchymal stem cells in mucolipidosis type II (I-cell disease)

dc.authoridköse, sevil/0000-0003-2188-9534
dc.authoridAerts Kaya, Fatima/0000-0002-9583-8572
dc.authoridÇetinkaya, Duygu Uçkan/0000-0003-3593-6493
dc.authorscopusid56494407000
dc.authorscopusid36439180500
dc.authorscopusid10338821200
dc.authorscopusid7004861894
dc.authorwosidköse, sevil/ABI-5227-2020
dc.authorwosidAerts Kaya, Fatima/ABG-1880-2020
dc.authorwosidÇetinkaya, Duygu Uçkan/X-2067-2019
dc.contributor.authorKöse, Sevil
dc.contributor.authorKaya, Fatima Aerts
dc.contributor.authorKuşkonmaz, Bülent Barış
dc.contributor.authorÇetinkaya, Duygu Uçkan
dc.contributor.otherNutrition and Dietetics
dc.date.accessioned2024-07-05T15:28:35Z
dc.date.available2024-07-05T15:28:35Z
dc.date.issued2019
dc.departmentAtılım Universityen_US
dc.department-tempATILIM ÜNİVERSİTESİ,HACETTEPE ÜNİVERSİTESİ,HACETTEPE ÜNİVERSİTESİ,HACETTEPE ÜNİVERSİTESİen_US
dc.descriptionköse, sevil/0000-0003-2188-9534; Aerts Kaya, Fatima/0000-0002-9583-8572; Çetinkaya, Duygu Uçkan/0000-0003-3593-6493en_US
dc.description.abstractMucolipidosis type II (ML-II, I-cell disease) is a fatal inherited lysosomal storage disease caused by a deficiency of theenzyme N-acetylglucosamine-1-phosphotransferase. A characteristic skeletal phenotype is one of the many clinical manifestationsof ML-II. Since the mechanisms underlying these skeletal defects in ML-II are not completely understood, we hypothesized that adefect in osteogenic differentiation of ML-II bone marrow mesenchymal stem cells (BM-MSCs) might be responsible for this skeletalphenotype. Here, we assessed and characterized the cellular phenotype of BM-MSCs from a ML-II patient before (BBMT) and afterBM transplantation (ABMT), and we compared the results with BM-MSCs from a carrier and a healthy donor. Morphologically, wedid not observe differences in ML-II BBMT and ABMT or carrier MSCs in terms of size or granularity. Osteogenic differentiation wasnot markedly affected by disease or carrier status. Adipogenic differentiation was increased in BBMT ML-II MSCs, but chondrogenicdifferentiation was decreased in both BBMT and ABMT ML-II MSCs. Immunophenotypically no significant differences were observedbetween the samples. Interestingly, the proliferative capacity of BBMT and ABMT ML-II MSCs was increased in comparison to MSCsfrom age-matched healthy donors. These data suggest that MSCs are not likely to cause the skeletal phenotype observed in ML-II, butthey may contribute to the pathogenesis of ML-II as a result of lysosomal storage-induced pathology.en_US
dc.description.sponsorshipTurkish Ministry for Development [2006-K120640]en_US
dc.description.sponsorshipThis study was supported by a grant from the Turkish Ministry for Development, PediSTEM No: 2006-K120640.en_US
dc.identifier.citation2
dc.identifier.doi10.3906/biy-1902-20
dc.identifier.endpage178en_US
dc.identifier.issn1300-0152
dc.identifier.issn1303-6092
dc.identifier.issue3en_US
dc.identifier.pmid31320815
dc.identifier.scopus2-s2.0-85071144231
dc.identifier.scopusqualityQ3
dc.identifier.startpage171en_US
dc.identifier.trdizinid336041
dc.identifier.urihttps://doi.org/10.3906/biy-1902-20
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/336041/characterization-of-mesenchymal-stem-cells-in-mucolipidosis-type-ii-i-cell-disease
dc.identifier.volume43en_US
dc.identifier.wosWOS:000471268100002
dc.identifier.wosqualityQ3
dc.institutionauthorKöse, Sevil
dc.language.isoenen_US
dc.publisherTubitak Scientific & Technological Research Council Turkeyen_US
dc.relation.ispartofTurkish Journal of Biologyen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectBiyolojien_US
dc.titleCharacterization of mesenchymal stem cells in mucolipidosis type II (I-cell disease)en_US
dc.typeArticleen_US
dspace.entity.typePublication
relation.isAuthorOfPublicationa114276c-9b58-4517-9fe0-170c501e8909
relation.isAuthorOfPublication.latestForDiscoverya114276c-9b58-4517-9fe0-170c501e8909
relation.isOrgUnitOfPublication2071c428-f13d-4e73-b6f2-9902e8f00103
relation.isOrgUnitOfPublication.latestForDiscovery2071c428-f13d-4e73-b6f2-9902e8f00103

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