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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
<?xml version='1.0' encoding='utf-8'?> <resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd"> <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> </alternateIdentifiers> <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> </rightsList> <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> </descriptions> </resource>
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