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婴儿无晶状体性青光眼:白细胞介素-4和血管内皮生长因子的潜在病因学作用

Infantile aphakic glaucoma: a proposed etiologic role of IL-4 and VEGF.

作者信息

Michael Inbal, Walton David S, Levenberg Shulamit

机构信息

Faculty of Bio-Medical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.

出版信息

J Pediatr Ophthalmol Strabismus. 2011 Mar-Apr;48(2):98-107. doi: 10.3928/01913913-20100518-04. Epub 2010 May 21.

DOI:10.3928/01913913-20100518-04
PMID:20506964
Abstract

PURPOSE

To identify the factors secreted by lens epithelial cells (LECs) responsible for the altered trabecular meshwork (TM) cells and to compare their effect on monocultured TM cells with that of TM cells co-cultured with LECs.

METHODS

Such factors were isolated using cytokine antibody array membranes, and their effect on TM cells was assessed by analyzing changes in morphology and gene expression. In addition, inhibition of the isolated factors was performed in the co-culture model by adding specific antibodies to the cell culture media.

RESULTS

Transforming growth factor beta-2, interleukin-4 (IL-4), and vascular endothelial growth factor (VEGF) are presented as candidate cytokines responsible for the observed changes in LEC-TM co-cultures. Culturing TM cells in the presence of VEGF and IL-4 triggered alterations closely reflecting those observed in the LEC-TM co-culture model, where their inhibition significantly hindered the alteration of the TM cells.

CONCLUSION

These findings suggest a possible explanation for the development of infantile aphakic glaucoma, based on residual LECs secreting IL-4 and VEGF after removal of congenital cataract, which then alter trabecular meshwork cell morphology and gene expression.

摘要

目的

鉴定晶状体上皮细胞(LECs)分泌的导致小梁网(TM)细胞改变的因子,并比较其对单培养TM细胞和与LECs共培养的TM细胞的影响。

方法

使用细胞因子抗体阵列膜分离这些因子,并通过分析形态和基因表达的变化来评估它们对TM细胞的影响。此外,在共培养模型中通过向细胞培养基中添加特异性抗体来抑制分离出的因子。

结果

转化生长因子β-2、白细胞介素-4(IL-4)和血管内皮生长因子(VEGF)被认为是导致LEC-TM共培养中观察到的变化的候选细胞因子。在VEGF和IL-4存在的情况下培养TM细胞会引发与LEC-TM共培养模型中观察到的变化密切相关的改变,在该模型中对它们的抑制显著阻碍了TM细胞的改变。

结论

这些发现为婴儿无晶状体性青光眼的发生提供了一种可能的解释,即先天性白内障摘除后残留的LECs分泌IL-4和VEGF,进而改变小梁网细胞的形态和基因表达。

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