UMSC 来源的外泌体促进视神经挤压大鼠模型中视网膜神经节细胞的存活。
UMSC-derived exosomes promote retinal ganglion cells survival in a rat model of optic nerve crush.
机构信息
Department of Ophthalmology, Changhai Hospital, Second Military Medical University School of Medicine, Shanghai, China; Department of Anatomy, Second Military Medical University School of Medicine, Shanghai, China; Department of Histology and Embryology, Second Military Medical University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Cell Engineering, Shanghai, China.
Department of Histology and Embryology, Second Military Medical University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Cell Engineering, Shanghai, China.
出版信息
J Chem Neuroanat. 2019 Mar;96:134-139. doi: 10.1016/j.jchemneu.2019.01.006. Epub 2019 Jan 10.
Traumatic optic neuropathy or glaucoma lead to retinal ganglion cells loss and cause blindness, and there is no effective therapy strategy by far. Mesenchymal cells from the Wharton's jelly of the umbilical cord (umbilical cord mesenchymal stem cells, UMSCs) and UMSC-derived exosomes (UMSC-Exos) are promising candidates for allogeneic therapy in regenerative medicine, but their effort on optic nerve injury and the underlying mechanism remains undefined. In the present study, we investigated the functions of UMSC-Exos in a rat optic nerve crush (ONC) model. After three times of treatments with an interval of one week, we found that the UMSC-Exos significantly promoted Brn3a retinal ganglion cells (RGCs) survival in retinal ganglion cell layer compared with PBS controls. UMSC-Exos also significantly promoted GFAP glia cells activation in retina and optic nerve. However, no increase of GAP43 axon counts in the optic nerve was found after UMSC-Exos treatment. Thus, our results demonstrate that UMSC-derived exosomes may play a role in neuroprotection by promoting the RGCs survival and glia cells activation but not the axon regeneration.
创伤性视神经病变或青光眼导致视网膜神经节细胞丧失，从而导致失明，目前尚无有效的治疗策略。脐带华通氏胶（脐带间充质干细胞，UMSC）中的间充质细胞和 UMSC 衍生的外泌体（UMSC-Exos）是再生医学中同种异体治疗的有前途的候选物，但它们在视神经损伤及其潜在机制方面的作用仍未确定。在本研究中，我们研究了 UMSC-Exos 在大鼠视神经挤压（ONC）模型中的作用。经过三次治疗，间隔一周，我们发现与 PBS 对照组相比，UMSC-Exos 显著促进了 Brn3a 视网膜神经节细胞（RGCs）在视网膜神经节细胞层中的存活。UMSC-Exos 还显著促进了视网膜和视神经中 GFAP 神经胶质细胞的激活。然而，在 UMSC-Exos 治疗后，视神经中的 GAP43 轴突计数并没有增加。因此，我们的结果表明，UMSC 衍生的外泌体可能通过促进 RGCs 存活和神经胶质细胞激活来发挥神经保护作用，但不能促进轴突再生。
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