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A possible mechanism of microglia-photoreceptor crosstalk
Yang, Li-ping1; Zhu, Xiu-an1; Tso, Mark O. M.1,2
刊名MOLECULAR VISION
2007-10-29
13期:231-32页:2048-2057
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Ophthalmology
研究领域[WOS]Biochemistry & Molecular Biology ; Ophthalmology
关键词[WOS]ACTIVATED PROTEIN-KINASE ; NF-KAPPA-B ; NITRIC-OXIDE SYNTHASE ; INDUCED RETINAL DEGENERATION ; CELL-DEATH ; NERVOUS-SYSTEM ; MAP KINASE ; RAT RETINA ; INDUCED APOPTOSIS ; IMMUNE-RESPONSES
英文摘要

Purpose: The goal of this study was to explore the relationship between photoreceptor apoptosis and retinal microglial activation.

Methods: A murine photoreceptor cell line (661W cells) was exposed to LPS-treated microglial cell conditioned medium (MGCM), and cell viability was assessed by terminal dUTP transferase nick end labeling ( TUNEL) and the 3-( 4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In addition, microglia were exposed to culture media from light-damaged 661W photoreceptor cells (PRCM), and microglial activation was assessed morphologically by phase contrast microscopy. Reverse transcription polymerase chain reaction was used to examine mRNA levels of several chemokines and noxious factors in the MGCM-treated photoreceptor cells and the PRCM-treated microgial. Western blotting was used to analyze NF-kappa B p65 subunit, phosphorylated MAPKs p38, p44/42 (Erk1/2), and c-Jun N-terminal kinase (JNK).

Results: Our results showed 37% of 661W cells underwent apoptosis following exposure to MGCM for 24 h. MGCM-induced death was associated with down-regulation of chemokine expression (i.e., eotaxin and RANTES), up-regulation of inflammatory mediators (i.e., MIP-1 alpha, MIP-1 beta, IL-10, iNOS, and TNF-alpha), and increased phosphorylation of p38, p44/p42, and JNK. Retinal microglia acquired an activated phenotype after exposure to PRCM for 24 h. Microglial activation was accompanied by increased NF-kappa B p65 expression, increased phosphorylation of p38 and JNK, and up-regulation of chemokines (i.e., eotaxin and RANTES) and inflammatory mediators (i.e., iNOS and IL-10).

Conclusions: Light-damaged photoreceptors release immunological signaling molecules that attract microglia, resulting in microglial activation and subsequent further degeneration of remaining photoreceptors. These results also suggest that p38, p44/42, and JNK may regulate glial-induced photoreceptor death and that p38, JNK, and NF-kappa B may regulate photoreceptor-induced microglial activation.

语种英语
WOS记录号WOS:000256545100002
引用统计
被引频次:30[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62515
专题北京大学第三临床医学院_眼科
作者单位1.Peking Univ, Peking Univ Hosp 3, Ctr Eye, Beijing 100083, Peoples R China
2.Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21205 USA
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GB/T 7714
Yang, Li-ping,Zhu, Xiu-an,Tso, Mark O. M.. A possible mechanism of microglia-photoreceptor crosstalk[J]. MOLECULAR VISION,2007,13(231-32):2048-2057.
APA Yang, Li-ping,Zhu, Xiu-an,&Tso, Mark O. M..(2007).A possible mechanism of microglia-photoreceptor crosstalk.MOLECULAR VISION,13(231-32),2048-2057.
MLA Yang, Li-ping,et al."A possible mechanism of microglia-photoreceptor crosstalk".MOLECULAR VISION 13.231-32(2007):2048-2057.
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