Inhibition by miR-410 facilitates direct retinal pigment epithelium differentiation of umbilical cord blood-derived mesenchymal stem cells

Retinal pigment epithelium (RPE) is a major component of the eye. This highly specialized cell type facilitates maintenance of the visual system. Because RPE loss induces an irreversible visual impairment, RPE generation techniques have recently been investigated as a potential therapeutic approach...

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Published inJournal of veterinary science (Suwŏn-si, Korea) Vol. 18; no. 1; pp. 59 - 65
Main Authors Choi, Soon Won, Kim, Jae-Jun, Seo, Min-Soo, Park, Sang-Bum, Shin, Tae-Hoon, Shin, Ji-Hee, Seo, Yoojin, Kim, Hyung-Sik, Kang, Kyung-Sun
Format Journal Article
LanguageEnglish
Published Korea (South) 대한수의학회 01.03.2017
The Korean Society of Veterinary Science
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Summary:Retinal pigment epithelium (RPE) is a major component of the eye. This highly specialized cell type facilitates maintenance of the visual system. Because RPE loss induces an irreversible visual impairment, RPE generation techniques have recently been investigated as a potential therapeutic approach to RPE degeneration. A microRNA-based technique is a new strategy for producing RPE cells from adult stem cell sources. Previously, we identified that antisense microRNA-410 (anti-miR-410) induces RPE differentiation from amniotic epithelial stem cells. In this study, we investigated RPE differentiation from umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs) via anti-miR-410 treatment. We identified miR-410 as a RPE-relevant microRNA in UCB-MSCs from among 21 putative human RPE-depleted microRNAs. Inhibition of miR-410 induces overexpression of immature and mature RPE-specific factors, including MITF, LRAT, RPE65, Bestrophin, and EMMPRIN. The RPE-induced cells were able to phagocytize microbeads. Results of our microRNA-based strategy demonstrated proof-of-principle for RPE differentiation in UCB-MSCs by using anti-miR-410 treatment without the use of additional factors or exogenous transduction.
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Present address: Department of Medical Science, School of Medicine, Pusan National University, Busan, Korea.
These authors contributed equally to this work.
Present address: Biomedical Research Institute, Pusan National University Hospital, Busan, Korea.
G704-001401.2017.18.1.008
http://www.vetsci.org/journal/download_pdf.php?doi=10.4142/jvs.2017.18.1.59
ISSN:1229-845X
1976-555X
DOI:10.4142/jvs.2017.18.1.59