Epithelium-derived miR-204 inhibits corneal neovascularization

Autor: Xiaoli Hu, Weiyun Shi, Guohu Di, Xiaoping Zhang, Xiaowen Zhao, Muchen Dong, Haoyun Duan, Mingli Qu, Ting Liu, Qingjun Zhou
Rok vydání: 2018
Předmět:
Male
Vascular Endothelial Growth Factor A
0301 basic medicine
Blotting
Western
In situ hybridization
Real-Time Polymerase Chain Reaction
Neovascularization
Mice
03 medical and health sciences
Cellular and Molecular Neuroscience
chemistry.chemical_compound
0302 clinical medicine
Cell Movement
Cornea
medicine
Animals
Corneal Neovascularization
Cells
Cultured
Cell Proliferation
Corneal epithelium
Tube formation
Mice
Inbred BALB C
Epithelium
Corneal
Endothelial Cells
medicine.disease
Immunohistochemistry
Vascular Endothelial Growth Factor Receptor-2
eye diseases
Sensory Systems
Epithelium
Vascular endothelial growth factor
Disease Models
Animal
MicroRNAs
Ophthalmology
030104 developmental biology
medicine.anatomical_structure
chemistry
Corneal neovascularization
030221 ophthalmology & optometry
Cancer research
Blood Vessels
sense organs
medicine.symptom
Zdroj: Experimental Eye Research. 167:122-127
ISSN: 0014-4835
DOI: 10.1016/j.exer.2017.12.001
Popis: MicroRNA-204 (miR-204) is highly expressed in cornea, here we explored the role and mechanism of miR-204 in corneal neovascularization (CNV). Mouse CNV was induced by intrastromal placement of suture in BALB/c mice with the subconjunctival injection of miR-204 agomir or negative control. Human primary limbal epithelial cells (LECs) and immortalized microvascular endothelial cells (HMECs) were used to evaluate the expression changes and anti-angiogenic effects of miR-204 under biomechanical stress (BS). The expression and localization of miR-204, vascular endothelial growth factor (VEGF) and their receptors were detected by quantitative real-time PCR, in situ hybridization, immunohistochemistry and Western blot. The results showed that miR-204 expression was mainly localized in epithelium and down-expressed in vascularized cornea. Subconjunctival injection of miR-204 agomir inhibited CNV and reduced the expression of VEGF and VEGF receptor 2. Similarly, miR-204 overexpression attenuated the increased expression of VEGF by biomechanical stress in LECs, and suppressed the proliferation, migration, and tube formation of HMECs. These novel findings indicate that epithelium-derived miR-204 inhibits suture-induced CNV through regulating VEGF and VEGF receptor 2.
Databáze: OpenAIRE
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