Inhibition by miR-410 facilitates direct retinal pigment epithelium differentiation of umbilical cord blood-derived mesenchymal stem cells
Inhibition by miR-410 facilitates direct retinal pigment epithelium differentiation of umbilical cord blood-derived mesenchymal stem cells
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DOI：
10.4142/jvs.2017.18.1.59
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发表时间：
2017-03-01
影响因子：
1.8
通讯作者：
Kang, Kyung-Sun
中科院分区：
文献类型：
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作者：
Choi, Soon Won;Kim, Jae-Jun;Kang, Kyung-Sun
视网膜色素上皮（RPE）是眼睛的主要组成部分。这种高度专业化的细胞类型有利于视觉系统的维护。由于 RPE 损失会导致不可逆的视力障碍，因此 RPE 生成技术最近被研究为 RPE 退化的潜在治疗方法。基于 microRNA 的技术是一种从成体干细胞来源生产 RPE 细胞的新策略。此前，我们发现反义 microRNA-410（抗 miR-410）可诱导羊膜上皮干细胞分化为 RPE。在这项研究中，我们通过抗 miR-410 治疗研究了脐带血来源的间充质干细胞 (UCB-MSC) 的 RPE 分化。我们从 21 种假定的人类 RPE 耗尽的 microRNA 中鉴定出 miR-410 是 UCB-MSC 中与 RPE 相关的 microRNA。抑制 miR-410 会诱导未成熟和成熟的 RPE 特异性因子过度表达，包括 MITF、LRAT、RPE65、Bestropin 和 EMMPRIN。 RPE 诱导的细胞能够吞噬微珠。我们基于 microRNA 的策略的结果证明了通过使用抗 miR-410 治疗而不使用其他因子或外源转导来实现 UCB-MSC 中 RPE 分化的原理验证。
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. The 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.