Generation and characterization of human induced pluripotent stem cells (iPSCs) from hand osteoarthritis patient-derived fibroblasts
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Identificadores
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Fecha de publicación
2020Título de revista
Scientific Reports
Tipo de contenido
Journal Article
DeCS
inmunohistoquímica | anciano | articulaciones de la mano | fibroblastos | huella del ADN | cariotipo | mediana edad | humanos | células | diferenciación celular | células madre pluripotentes inducidas | osteoartritis | condrogénesisMeSH
Middle Aged | Hand Joints | Osteoarthritis | Induced Pluripotent Stem Cells | Cell Differentiation | Immunohistochemistry | Chondrogenesis | Humans | Fibroblasts | Cells | Karyotype | DNA Fingerprinting | AgedResumen
Knowledge and research results about hand osteoarthritis (hOA) are limited due to the lack of samples and animal models of the disease. Here, we report the generation of two induced pluripotent stem cell (iPSC)-lines from patients with radiographic hOA. Furthermore, we wondered whether these iPSC-lines carried single nucleotide polymorphisms (SNPs) within genes that have been associated with hOA. Finally, we performed chondrogenic differentiation of the iPSCs in order to prove their usefulness as cellular models of the disease. We performed a non-integrative reprogramming of dermal fibroblasts obtained from two patients with radiographic rhizarthrosis and non-erosive hOA by introducing the transcriptional factors Oct4, Sox2, Klf4 and c-Myc using Sendai virus. After reprogramming, embryonic stem cell-like colonies emerged in culture, which fulfilled all the criteria to be considered iPSCs. Both iPSC-lines carried variants associated with hOA in the four studied genes and showed differences in their chondrogenic capacity when compared with a healthy control iPSC-line. To our knowledge this is the first time that the generation of iPSC-lines from patients with rhizarthrosis and non-erosive hOA is reported. The obtained iPSC-lines might enable us to model the disease in vitro, and to deeper study both the molecular and cellular mechanisms underlying hOA.
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