scholarly journals Tetramethylpyrazine in a Murine Alkali-Burn Model Blocks NFκB/NRF-1/CXCR4-Signaling-Induced Corneal Neovascularization

2018 ◽  
Vol 59 (5) ◽  
pp. 2133 ◽  
Author(s):  
Mingjun Tang ◽  
Ying Yang ◽  
Jingzhi Yu ◽  
Jin Qiu ◽  
Pei Chen ◽  
...  
Keyword(s):  
Corneal Neovascularization ◽  
Cxcr4 Signaling ◽  
Alkali Burn

Inhibitory Effect of Canstatin in Alkali Burn-Induced Corneal Neovascularization

2011 ◽  
Vol 46 (2) ◽  
pp. 66-72 ◽  
Author(s):  
Ye Wang ◽  
Hongmei Yin ◽  
Peng Chen ◽  
Lixin Xie ◽  
Yiqiang Wang
Keyword(s):  
Corneal Neovascularization ◽  
Inhibitory Effect ◽  
Alkali Burn

Suppression of Alkali Burn-Induced Corneal Neovascularization by Dendritic Cell Vaccination Targeting VEGF Receptor 2

2008 ◽  
Vol 49 (5) ◽  
pp. 2172 ◽  
Author(s):  
Hiroshi Mochimaru ◽  
Tomohiko Usui ◽  
Tomonori Yaguchi ◽  
Yasuharu Nagahama ◽  
Go Hasegawa ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Corneal Neovascularization ◽  
Dendritic Cell Vaccination ◽  
Vegf Receptor ◽  
Alkali Burn

scholarly journals G9a Suppression Alleviates Corneal Neovascularization through Blocking Nox4-Mediated Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Shanshan Wan ◽  
Wanju Yang ◽  
Yumiao Pan ◽  
Zhuoqun Rao ◽  
Yanning Yang
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Corneal Neovascularization ◽  
Ros Production ◽  
Corneal Injury ◽  
Alkali Burn ◽  
Nadph Oxidase 4

Background. G9a, a well-known methyltransferase, plays a vital role in biological processes. However, its role in corneal neovascularization (CoNV) remains unclear. Methods. In vitro and in vivo models were assessed in hypoxia-stimulated angiogenesis and in a mouse model of alkali burn-induced CoNV. Human umbilical vein endothelial cells (HUVECs) were cultured under hypoxic conditions and different reoxygenation times to identify the molecular mechanisms involved in this process. Results. In this study, we found that G9a was positively related to corneal alkali burn-induced injury. Inhibition of G9a with BIX 01294 (BIX) alleviated corneal injury, including oxidative stress and neovascularization in vivo. Similarly, inhibition of G9a with either BIX or small interfering RNA (siRNA) exerted an inhibitory effect on hypoxia/reoxygenation (H/R)-induced oxidative stress and angiogenesis in HUVECs. Moreover, our study revealed that ablation of reactive oxygen species (ROS) with N-acetyl-cysteine suppressed angiogenesis in HUVECs exposed to H/R stimulation. Furthermore, NADPH oxidase 4 (Nox4), which was positively associated with ROS production and angiogenesis, was elevated during H/R. This effect could be reversed through suppression of the transcription activity of G9a with BIX or siRNA. In addition, the Nrf2/HO-1 pathway, upstream of Nox4, was activated in both BIX-treated mice and G9a-inhibited HUVECs. Collectively, our results demonstrated that inhibition of G9a-alleviated corneal angiogenesis by inhibiting Nox4-dependent ROS production through the Nrf2/HO-1 signaling pathway. These findings indicate that G9a may be a valuable therapeutic target for CoNV.

Inhibitory Effect of Sub-conjunctival Tocilizumab on Alkali Burn Induced Corneal Neovascularization in Rats

2014 ◽  
Vol 40 (1) ◽  
pp. 48-55 ◽  
Author(s):  
Esin Sogutlu Sari ◽  
Alper Yazıcı ◽  
Hasan Aksit ◽  
Arzu Yay ◽  
Gözde Sahin ◽  
...  
Keyword(s):  
Corneal Neovascularization ◽  
Inhibitory Effect ◽  
Alkali Burn

Plasminogen Kringle 5 Inhibits Alkali-Burn–Induced Corneal Neovascularization

2005 ◽  
Vol 46 (11) ◽  
pp. 4062 ◽  
Author(s):  
Zhihong Zhang ◽  
Jian-xing Ma ◽  
Guoquan Gao ◽  
Chaoyang Li ◽  
Lihui Luo ◽  
...  
Keyword(s):  
Corneal Neovascularization ◽  
Alkali Burn ◽  
Kringle 5

scholarly journals Tetramethylpyrazine (TMP) ameliorates corneal neovascularization via regulating cell infiltration into cornea after alkali burn

2019 ◽  
Vol 109 ◽  
pp. 1041-1051 ◽  
Author(s):  
Yihui Wu ◽  
Zhuojun Xu ◽  
Ying Yang ◽  
Jin Qiu ◽  
Meng Yang ◽  
...  
Keyword(s):  
Corneal Neovascularization ◽  
Cell Infiltration ◽  
Alkali Burn

Bevacizumab inhibits corneal neovascularization in an alkali burn induced model of corneal angiogenesis

2007 ◽  
Vol 35 (8) ◽  
pp. 745-748 ◽  
Author(s):  
Hamid Hosseini ◽  
Mahmood Nejabat ◽  
Morsal Mehryar ◽  
Taher Yazdchi ◽  
Ahad Sedaghat ◽  
...  
Keyword(s):  
Corneal Neovascularization ◽  
Alkali Burn ◽  
Corneal Angiogenesis

scholarly journals Effect of Collagen Cross-Linking on Alkali Burn-Induced Corneal Neovascularization in Rabbits

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Xiaoying Xu ◽  
Taixiang Liu ◽  
Haixiang Li
Keyword(s):  
Corneal Edema ◽  
Corneal Neovascularization ◽  
Matrix Metalloproteinase 2 ◽  
Cross Linking ◽  
Ultraviolet A ◽  
Treatment Groups ◽  
Alkali Burn ◽  
Group A ◽  
Collagen Cross Linking ◽  
Corneal Collagen

Objective. This study aims at investigating the effects and molecular mechanism of riboflavin-ultraviolet-A-induced cross-linking (corneal collagen cross-linking, CXL) on corneal neovascularization (CNV) in a rabbit alkali burn model. Methods. A total of 60 rabbits were injured with alkali burns to induce CNV in the right eye and were randomly divided into six groups: Group A—injury and no treatment; Groups B, C, and D—CXL treatment for 30 min, 15 min, and 45 min administered immediately after injury, respectively; and Groups E and F—CXL treatment for 30 min administered 1 day and 3 days after injury, respectively. CNV area, corneal edema, and corneal epithelial defects were observed on days 4, 7, 10, and 14 after injury. Western blot was used to detect expression of the vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-2 (MMP-9), and tissue inhibitor of metalloproteinases 1 (TIMP-1) at 7 and 14 days after injury. Results. CXL treatment decreased CNV and corneal edema in all groups compared to Group A. On day 7, MMP-9 expression was significantly increased in all CXL treatment groups, and TIMP-1 was upregulated in Groups D and F compared to Group A. In addition, VEGF, MMP-2, MMP-9, and TIMP-1 expression were increased in Group A on day 14 after injury. Conclusions. Our results indicate that riboflavin-ultraviolet-A-induced cross-linking (corneal collagen cross-linking, CXL) significantly inhibits alkali burn-induced CNV in rabbits, possibly through downregulating VEGF, MMP-2, MMP-9, and TIMP-1 expression.

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