Attenuation of periostin in retinal Müller glia by TNF-αand IFN-γ

• 作者: Hui-Lan Zeng Jing-Ling Zou Jing-Ming Shi Lu-Si Zhang Man-Jing Cao Shigeo Yoshida Song-Bai Jia Takahito Nakama Ye-Di Zhou Ying-Qian Peng Yoshiyuki Kobayashi
• 来源期刊: 国际眼科杂志:英文版
• 学科: 医学
• 关键词: TNF-Α IFN-Γ PERIOSTIN Müller GLIA RETINAL neovascularization
• 年，卷（期）: 2019,（2）
• 页码范围: 212-218
• 页数: 7页
• 分类号: R783.2

摘要

AIM:To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS:The oxygen-induced retinopathy(OIR) mouse model and the human Moorfield/Institute of Ophthalmology-Müller 1(MIO-M1) cell line were used in the study. Immunofluorescence staining was used to determine the distribution and expression of periostin and a Müller glial cell marker glutamine synthetase(GS). Cytokines TNF-α and IFN-γ were added to stimulate the MIO-M1 cells. ShRNA was used to knockdown periostin expression in MIO-M1 cells. Quantitative real-time reverse transcription polymerase chain reaction(qRT-PCR) was conducted to assess the mRNA expression of periostin. RESULTS:Immunofluorescence staining showed that periostin was expressed by MIO-M1 Müller glia. GS-positive Müller glia and periostin increased in OIR retinas, and were partially overlaid. The stimulation of TNF-α and IFN-γ reduced the mRNA expression of periostin significantly and dose-dependently in MIO-M1 cells. Knockdown of periostin reduced mRNA expression of vascular endothelial growth factor A(VEGFA) in MIO-M1 cells, while VEGFA expression was not changed in periostin knock-out OIR retinas. CONCLUSION:Müller glia could be one of the main sources of periostin in the retina, and might contribute to the pathogenesis of retinal neovascularization. Proinflammatory cytokines TNF-α and IFN-γ attenuate the periostin expression in retinal Müller glia, which provides a potential and novel method in treating retinal neovascular diseases.