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Cagnan, Ilgin; Keles, Mustafa; Keskus, Ayse Gokce; Tombaz, Melike; Sahan, Ozge Burcu; Aerts-Kaya, Fatima; Uckan-Cetinkaya, Duygu; Konu, Ozlen; Gunel-Ozcan, Aysen
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<identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/238442</identifier>
<creators>
<creator>
<creatorName>Cagnan, Ilgin</creatorName>
<givenName>Ilgin</givenName>
<familyName>Cagnan</familyName>
</creator>
<creator>
<creatorName>Keles, Mustafa</creatorName>
<givenName>Mustafa</givenName>
<familyName>Keles</familyName>
</creator>
<creator>
<creatorName>Keskus, Ayse Gokce</creatorName>
<givenName>Ayse Gokce</givenName>
<familyName>Keskus</familyName>
<affiliation>Bilkent Univ, Interdisciplinary Neurosci Program, Ankara, Turkey</affiliation>
</creator>
<creator>
<creatorName>Tombaz, Melike</creatorName>
<givenName>Melike</givenName>
<familyName>Tombaz</familyName>
<affiliation>Bilkent Univ, Dept Mol Biol & Genet, Ankara, Turkey</affiliation>
</creator>
<creator>
<creatorName>Sahan, Ozge Burcu</creatorName>
<givenName>Ozge Burcu</givenName>
<familyName>Sahan</familyName>
</creator>
<creator>
<creatorName>Aerts-Kaya, Fatima</creatorName>
<givenName>Fatima</givenName>
<familyName>Aerts-Kaya</familyName>
</creator>
<creator>
<creatorName>Uckan-Cetinkaya, Duygu</creatorName>
<givenName>Duygu</givenName>
<familyName>Uckan-Cetinkaya</familyName>
</creator>
<creator>
<creatorName>Konu, Ozlen</creatorName>
<givenName>Ozlen</givenName>
<familyName>Konu</familyName>
</creator>
<creator>
<creatorName>Gunel-Ozcan, Aysen</creatorName>
<givenName>Aysen</givenName>
<familyName>Gunel-Ozcan</familyName>
</creator>
</creators>
<titles>
<title>Global Mirna Expression Of Bone Marrow Mesenchymal Stem/Stromal Cells Derived From Fanconi Anemia Patients</title>
</titles>
<publisher>Aperta</publisher>
<publicationYear>2022</publicationYear>
<dates>
<date dateType="Issued">2022-01-01</date>
</dates>
<resourceType resourceTypeGeneral="Text">Journal article</resourceType>
<alternateIdentifiers>
<alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/238442</alternateIdentifier>
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<relatedIdentifiers>
<relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1007/s13577-021-00626-9</relatedIdentifier>
</relatedIdentifiers>
<rightsList>
<rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
<rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
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<descriptions>
<description descriptionType="Abstract">Fanconi anemia (FA) is a rare genetic disorder characterized by genomic instability, developmental defects, and bone marrow (BM) failure. Hematopoietic stem cells (HSCs) in BM interact with the mesenchymal stem/stromal cells (MSCs); and this partly sustains the tissue homeostasis. MicroRNAs (miRNAs) can play a critical role during these interactions possibly via paracrine mechanisms. This is the first study addressing the miRNA profile of FA BM-MSCs obtained before and after BM transplantation (preBMT and postBMT, respectively). Non-coding RNA expression profiling and quality control analyses were performed in Donors (n = 13), FA preBMT (n = 11), and FA postBMT (n = 6) BM-MSCs using GeneChip miRNA 2.0 Array. Six Donor-FA preBMT pairs were used to identify a differentially expressed miRNA expression signature containing 50 miRNAs, which exhibited a strong correlation with the signature obtained from unpaired samples. Five miRNAs (hsa-miR-146a-5p, hsa-miR-148b-3p, hsa-miR-187-3p, hsa-miR-196b-5p, and hsa-miR-25-3p) significantly downregulated in both the paired and unpaired analyses were used to generate the BM-MSCs' miRNA-BM mononuclear mRNA networks upon integration of a public dataset (GSE16334; studying Donor versus FA samples). Functionally enriched KEGG pathways included cellular senescence, miRNAs, and pathways in cancer. Here, we showed that hsa-miR-146a-5p and hsa-miR-874-3p were rescued upon BMT (n = 3 triplets). The decrease in miR-146a-5p was also validated using RT-qPCR and emerged as a strong candidate as a modulator of BM mRNAs in FA patients.</description>
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