Department of Physiological Genomics, Biomedical Center, Ludwig-Maximilians-Universität München, D-82152 Planegg-Martinsried, Germany.
Laboratory for Experimental Immunology of the Eye, Department of Ophthalmology, Faculty of Medicine and University Hospital Cologne, University of Cologne, D-50931 Cologne, Germany.
Int J Mol Sci. 2021 Jan 25;22(3):1174. doi: 10.3390/ijms22031174.
Müller cells, the major retinal macroglia, are key to maintaining vascular integrity as well as retinal fluid and ion homeostasis. Although platelet derived growth factor (PDGF) receptor expression in Müller glia has been reported earlier, their actual role for Müller cell function and intimate interaction with cells of the retinal neurovascular unit remains unclear. To close this gap of knowledge, Müller cell-specific PDGF receptor alpha (PDGFRα) knockout (KO) mice were generated, characterized, and subjected to a model of choroidal neovascularization (CNV). PDGFRα-deficient Müller cells could not counterbalance hypoosmotic stress as efficiently as their wildtype counterparts. In wildtypes, the PDGFRα ligand PDGF-BB prevented Müller cell swelling induced by the administration of barium ions. This effect could be blocked by the PDGFR family inhibitor AC710. PDGF-BB could not restore the capability of an efficient volume regulation in PDGFRα KO Müller cells. Additionally, PDGFRα KO mice displayed reduced rod and cone-driven light responses. Altogether, these findings suggest that Müller glial PDGFRα is central for retinal functions under physiological conditions. In contrast, Müller cell-specific PDGFRα KO resulted in less vascular leakage and smaller lesion areas in the CNV model. Of note, the effect size was comparable to pharmacological blockade of PDGF signaling alone or in combination with anti-vascular endothelial growth factor (VEGF) therapy-a treatment regimen currently being tested in clinical trials. These data imply that targeting PDGF to treat retinal neovascular diseases may have short-term beneficial effects, but may elicit unwarranted side effects given the putative negative effects on Müller cell homeostatic functions potentially interfering with a long-term positive outcome.
Müller 细胞是视网膜的主要胶质细胞,对维持血管完整性以及视网膜液体和离子平衡至关重要。尽管以前曾报道过血小板衍生生长因子 (PDGF) 受体在 Müller 胶质细胞中的表达,但它们对 Müller 细胞功能的实际作用以及与视网膜神经血管单元细胞的密切相互作用仍不清楚。为了弥补这一知识空白,生成了 Müller 细胞特异性 PDGF 受体α (PDGFRα) 敲除 (KO) 小鼠,并对其进行了脉络膜新生血管 (CNV) 模型的研究。PDGFRα 缺失的 Müller 细胞无法像其野生型对应物那样有效地对抗低渗应激。在野生型中,PDGFRα 配体 PDGF-BB 可防止 PDGF-BB 防止由钡离子给药引起的 Müller 细胞肿胀。该作用可被 PDGFR 家族抑制剂 AC710 阻断。PDGF-BB 不能恢复 PDGFRα KO Müller 细胞中有效的体积调节能力。此外,PDGFRα KO 小鼠的光感受器驱动的光反应减少。总而言之,这些发现表明 Müller 胶质细胞 PDGFRα 在生理条件下对视网膜功能至关重要。相反,在 CNV 模型中,Müller 细胞特异性 PDGFRα KO 导致血管渗漏减少和病变面积减小。值得注意的是,这种作用大小与 PDGF 信号的单独药理学阻断或与抗血管内皮生长因子 (VEGF) 治疗相结合相当,这是目前正在临床试验中测试的一种治疗方案。这些数据表明,针对 PDGF 治疗视网膜新生血管疾病可能具有短期的有益效果,但鉴于对 Müller 细胞稳态功能的潜在负面影响,可能会引起不必要的副作用,从而对长期的积极结果产生影响。