C57Bl6J retina lysates

Diabetic retinopathy (DR) is one of the main causes of blindness in working age populations in industrialized countries. It is estimated that close to 100 million individuals worldwide suffer from DR. Regrettably, relatively little is known of the cellular processes at play during late stages of the disease, especially concerning diabetic macular edema (DME). Streptozotocin-induced diabetic retinopathy (STZ) allows to reproduce experimentally in the mouse retina the retina vascular leakage and neuroegeneration features observed in human pathological retina with non-proliferative DR. Using agnostic and orthogonal approaches, in our work we demonstrate that in contrast to healthy retina, the STZ diabetic retina engages pathways of cell cycle arrest, resulting in cellular senescence. These findings combined with further pharmacological approaches provide mechanistic evidence supporting that targeting selectively senescent vessels in DR represents a potential treatment for high vascular permeability in DME. Overall design: 2 samples were analyzed: control citrate (2 replicates), streptozotocin-induced diabetes or STZ (2 replicates)糖尿病视网膜病变（Diabetic retinopathy, DR）是工业化国家劳动年龄人群失明的主要诱因之一。据估算，全球近1亿人群罹患糖尿病视网膜病变。遗憾的是，目前学界对该疾病晚期阶段发挥作用的细胞过程仍所知甚少，尤其针对糖尿病黄斑水肿（Diabetic macular edema, DME）的相关研究更为匮乏。链脲佐菌素诱导的糖尿病视网膜病变（Streptozotocin-induced diabetic retinopathy, STZ）模型可在小鼠视网膜中实验性重现人类非增殖性糖尿病视网膜病变患者病变视网膜所呈现的血管渗漏与神经退行性变特征。本研究采用无偏且正交的研究策略，证实相较于健康视网膜，STZ诱导的糖尿病视网膜会激活细胞周期阻滞通路，进而引发细胞衰老。结合后续药理学实验手段，上述研究结果提供了机制层面的证据，支持选择性靶向糖尿病视网膜病变中的衰老血管，可作为改善糖尿病黄斑水肿高血管通透性问题的潜在治疗方案。实验设计概述：本研究共分析2组样本，分别为柠檬酸盐对照（2个生物学重复）、链脲佐菌素诱导糖尿病组（简称STZ组，2个生物学重复）。