Limited Hyperoxia-Induced Proliferative Retinopathy (LHIPR) as a Model of Retinal Fibrosis, Angiogenesis, and Inflammation.
Limited Hyperoxia-Induced Proliferative Retinopathy (LHIPR) as a Model of Retinal Fibrosis, Angiogenesis, and Inflammation.
复制标题
高氧诱导的增生性视网膜病（LHIPR）是视网膜纤维化，血管生成和炎症的模型。
作者：
早产儿视网膜病变（ROP）和其他缺血性视网膜病变的纤维化和牵引进展仍然是一个重要的临床和手术挑战，需要全面了解其发病机制。纤维化是细胞外基质成分的不平衡沉积，其导致瘢痕组织形成，并随之导致组织和器官损伤。视网膜脱离是视网膜脱离的主要原因之一。我们利用有限高氧诱导的视网膜病变（LHIPR）模型，因为它反映了在ROP和其他缺血性视网膜病变中观察到的更高级的病理表型。为了模拟LHIPR，我们将野生型C57 B1/6 J小鼠幼仔从P0至P7暴露于65%氧气。然后，将幼仔放回室内空气中恢复，直至随后的终点。我们进行了组织学和分子分析，以评估纤维化进展，血管生成和炎症在几个时间点，从1.5个月到9个月。此外，我们通过光学相干断层扫描（OCT）或OCT血管造影（OCTA）进行体内视网膜成像，以跟踪体内纤维血管进展。虽然视网膜形态相对保存，我们发现随着时间的推移，视网膜前纤维化逐渐增加，直到9个月大。我们还检测到视网膜前间隙中的血管以及活跃的炎症过程，完全模仿人类的晚期视网膜前纤维血管病。
The progression to fibrosis and traction in retinopathy of prematurity (ROP) and other ischemic retinopathies remains an important clinical and surgical challenge, necessitating a comprehensive understanding of its pathogenesis. Fibrosis is an unbalanced deposition of extracellular matrix components responsible for scar tissue formation with consequent tissue and organ impairment. Together with retinal traction, it is among the main causes of retinal detachment and vision loss. We capitalize on the Limited Hyperoxia Induced Retinopathy (LHIPR) model, as it reflects the more advanced pathological phenotypes seen in ROP and other ischemic retinopathies. To model LHIPR, we exposed wild-type C57Bl/6J mouse pups to 65% oxygen from P0 to P7. Then, the pups were returned to room air to recover until later endpoints. We performed histological and molecular analysis to evaluate fibrosis progression, angiogenesis, and inflammation at several time points, from 1.5 months to 9 months. In addition, we performed in vivo retinal imaging by optical coherence tomography (OCT) or OCT Angiography (OCTA) to follow the fibrovascular progression in vivo. Although the retinal morphology was relatively preserved, we found a progressive increase in preretinal fibrogenesis over time, up to 9 months of age. We also detected blood vessels in the preretinal space as well as an active inflammatory process, altogether mimicking advanced preretinal fibrovascular disease in humans.
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