Abstract
ObjectivesTo treat traumatic optic neuropathy (TON) with transplantation of human umbilical cord blood stem cells (hUCBSC) and explore how transplanted stem cells participate in the neuron repairing process.MethodsA total of 195 Sprague-Dawley rats were randomly assigned to three groups: sham-surgery, optic nerve injury, and stem cell transplant group. Optic nerve injury was established in rats by directly clamping the optic nerve for 30 seconds. hUCBSC was microinjected into the vitreous cavity of injured rats. Optic nerve function was evaluated by flash visual evoked potentials (F-VEP). Apoptosis in retina tissues was detected by TUNEL staining. GRP78 and CHOP gene expression was measured by RT-PCR.ResultsAfter injury, transplantation of hUCBSC significantly blunted a reduction in optic nerve function indicated by smaller decreases in amplitude and smaller increases in peak latency of F-VEP waveform compared to the injury alone group. Also, significant more in retinal ganglion cell (RGC) count and less in RGC apoptosis were detected after transplantation compared to injured rats. The protective effect correlated with upregulated GRP78 and downregulated CHOP mRNA expression.ConclusionIntravitreal transplantation of hUCBSCs significantly blunted a reduction in optic nerve function through increasing RGC survival and decreasing retinal cell apoptosis. The protective role of transplantation was associated with upregulation of GRP78 expression and downregulation of CHOP expression in retinal cells.
Highlights
Traumatic optic neuropathy (TON) is an important cause of severe vision loss in 0.5 to 5% of patients with closed head trauma [1]
We investigated the protective mechanism by examining neuron apoptosis, GRP78, and CHOP expression in human umbilical cord blood stem cells (hUCBSC) transplanted retina compared to the injured retina without transplantation
flash visual evoked potentials (F-VEP) graphics showed that in the sham-surgery group, FVEP waveform was stable (Figure 1A) and no significant change was observed with time
Summary
Traumatic optic neuropathy (TON) is an important cause of severe vision loss in 0.5 to 5% of patients with closed head trauma [1]. Trauma causes immediate mechanical damage to a fraction of retinal ganglion cell (RGC) axons, which becomes irreversible during subsequent RGC degeneration. Following the initial damage to the optic nerve, swelling within the optic nerve canal or compression by bone fragments may lead to secondary RGC loss [2]. This secondary damage further impairs the already compromised blood supply to surviving RGCs, and subsequently causes apoptotic cell death [2]. A variety of treatments including conservative management, steroids application, surgical decompression, and a combination of surgery and steroid treatment have been used to prevent pathological damages to the optic nerves and increase retinal ganglion cell (RGC) survival post trauma. Using stem cells to replace lost neuron cells is a promising strategy that has been developed recently
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