Streptozotocin‑induced diabetic mice exhibit reduced experimental choroidal neovascularization but not corneal neovascularization.

Streptozotocin‑induced diabetic mice exhibit reduced experimental choroidal neovascularization but not corneal neovascularization.
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链脲佐菌素诱导的糖尿病小鼠表现出实验性脉络膜新生血管减少,但角膜新生血管没有减少

DOI:
10.3892/mmr.2018.9445
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发表时间:
2018-11
影响因子:
3.4
通讯作者:
Lu P
Lu P
中科院分区:
医学4区
文献类型:
--
作者:
Liu G;Chen L;Cai Q;Wu H;Chen Z;Zhang X;Lu P

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本研究旨在探讨糖尿病(DM)对实验性角膜新生血管(CrNV)和脉络膜新生血管(ChNV)的影响。用链脲佐菌素(STZ)诱导小鼠糖尿病模型。分别用碱伤法和激光光凝法诱导实验性CrNV和CHNV。损伤后2周比较STZ诱导的糖尿病小鼠和对照组小鼠的CrNV和ChNV。用逆转录-定量聚合酶链式反应检测血管生成因子的相对表达,用流式细胞仪检测损伤后早期祖细胞或巨噬细胞的聚集情况。与碱损伤正常小鼠相比,碱损伤糖尿病小鼠(STZ诱导)的CrNV发生率无显著差异,而激光损伤糖尿病小鼠的ChNV水平明显低于激光损伤对照组动物。激光诱导糖尿病小鼠血管内皮生长因子、缺氧诱导因子-1α、趋化因子(C-C基序)配体3和基质细胞衍生因子-1α的表达水平低于激光损伤对照组。此外,激光损伤的糖尿病小鼠与激光损伤的对照组小鼠相比,激光诱导的c-Kit+祖细胞在脉络膜内的渗透受到损害。总体而言,糖尿病对实验性CrNV的产生没有显著影响。然而,糖尿病通过下调脉络膜前体细胞的浸润和血管生成因子的表达来减少激光诱导的CHNV。
The present study aimed to investigate the effects of diabetes mellitus (DM) on the generation of experimental corneal neovascularization (CrNV) and choroidal neovascularization (ChNV). Diabetes was induced in mice by intraperitoneal injection of streptozotocin (STZ). Experimental CrNV and ChNV were induced by alkali injury and laser photocoagulation, respectively. CrNV and ChNV were compared between the STZ-induced diabetic mice and control mice two weeks after injury. Relative expression of angiogenic factors was quantified by reverse transcription-quantitative polymerase chain reaction, and progenitor cell or macrophage accumulation in the early phase following injury was examined by flow cytometric analysis. Compared with the alkali-injured normal mice, the alkali-injured diabetic mice (STZ-induced) exhibited no significant difference in CrNV occurrence, whereas the laser-injured diabetic mice exhibited significantly reduced levels of ChNV compared with those of the laser-injured control animals. The laser-induced intrachoroidal mRNA expression levels of angiogenic factors, including vascular endothelial growth factor, hypoxia-induced factor-1α, chemokine (C-C motif) ligand 3, and stromal cell-derived factor-1α, were reduced in the laser-injured diabetic mice when compared with laser-injured control mice. Furthermore, the laser-induced intrachoroidal infiltration of c-Kit+ progenitor cells was impaired in the laser-injured diabetic mice compared with the laser-injured control mice. Overall, diabetes did not exert a significant effect on the generation of experimental CrNV. However, diabetes reduced laser-induced ChNV through downregulation of intrachoroidal progenitor cell infiltration and angiogenic factor expression.
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