Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center, AA7103 MCN/VUIIS, 1161 21st Ave. S., Nashville, TN 37232, USA.
Stuart Therapeutics, Inc., 411 SE Osceola St., Suite 203, Stuart, FL 34994, USA.
Int J Mol Sci. 2022 Mar 8;23(6):2911. doi: 10.3390/ijms23062911.
Vision loss through the degeneration of retinal ganglion cell (RGC) axons occurs in both chronic and acute conditions that target the optic nerve. These include glaucoma, in which sensitivity to intraocular pressure (IOP) causes early RGC axonal dysfunction, and optic nerve trauma, which causes rapid axon degeneration from the site of injury. In each case, degeneration is irreversible, necessitating new therapeutics that protect, repair, and regenerate RGC axons. Recently, we demonstrated the reparative capacity of using collagen mimetic peptides (CMPs) to heal fragmented collagen in the neuronal extracellular milieu. This was an important step in the development of neuronal-based therapies since neurodegeneration involves matrix metalloproteinase (MMP)-mediated remodeling of the collagen-rich environment in which neurons and their axons exist. We found that intraocular delivery of a CMP comprising single-strand fractions of triple helix human type I collagen prevented early RGC axon dysfunction in an inducible glaucoma model. Additionally, CMPs also promoted neurite outgrowth from dorsal root ganglia, challenged in vitro by partial digestion of collagen. Here, we compared the ability of a CMP sequence to protect RGC axons in both inducible glaucoma and optic nerve crush. A three-week +40% elevation in IOP caused a 67% degradation in anterograde transport to the superior colliculus, the primary retinal projection target in rodents. We found that a single intravitreal injection of CMP during the period of IOP elevation significantly reduced this degradation. The same CMP delivered shortly after optic nerve crush promoted significant axonal recovery during the two-week period following injury. Together, these findings support a novel protective and reparative role for the use of CMPs in both chronic and acute conditions affecting the survival of RGC axons in the optic projection to the brain.
视网膜神经节细胞 (RGC) 轴突的退化导致视力丧失,这种情况既发生于慢性条件下,也发生于急性条件下,且均会影响视神经。这些情况包括青光眼,其特征是对眼内压 (IOP) 的敏感性导致早期 RGC 轴突功能障碍,以及视神经损伤,其导致从损伤部位快速的轴突退化。在每种情况下,退化都是不可逆转的,这就需要新的治疗方法来保护、修复和再生 RGC 轴突。最近,我们证明了使用胶原蛋白模拟肽 (CMP) 修复神经元细胞外基质中碎片化胶原蛋白的修复能力。这是神经元为基础的治疗方法发展的重要一步,因为神经退行性变涉及到基质金属蛋白酶 (MMP) 介导的富含胶原蛋白的环境重塑,神经元及其轴突存在于该环境中。我们发现,在可诱导的青光眼模型中,眼内注射由三螺旋人 I 型胶原蛋白单链片段组成的 CMP 可防止早期 RGC 轴突功能障碍。此外,CMP 还促进了背根神经节的神经突生长,在体外受到胶原蛋白部分消化的挑战。在这里,我们比较了 CMP 序列在可诱导性青光眼和视神经挤压两种情况下保护 RGC 轴突的能力。IOP 升高 40%持续 3 周导致顺行运输到上丘(啮齿动物的主要视网膜投射靶标)的降解达到 67%。我们发现,在 IOP 升高期间单次玻璃体内注射 CMP 可显著降低这种降解。在视神经挤压后不久给予相同的 CMP,可促进损伤后两周内的显著轴突恢复。总之,这些发现支持在影响视神经投射到大脑的 RGC 轴突存活的慢性和急性情况下使用 CMP 具有新的保护和修复作用。