排序方式: 共有78条查询结果,搜索用时 234 毫秒
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Age-related macular degeneration: activation of innate immunity system via pattern recognition receptors 总被引:1,自引:0,他引:1
Age-related macular degeneration (AMD) is the most common cause of irreversible loss of central vision. Histopathological
studies have demonstrated that inflammation is the key player in the pathogenesis of AMD. Genetic studies have revealed that
complement factor H is a strong risk factor for the development of AMD. However, innate immunity defence involves several
other pattern recognition receptors (PRRs) which can trigger inflammatory responses. Retinal pigment epithelial (RPE) cells
have the main role in the immune defence in macula. In this study, we examine in detail the endogenous danger signals which
can activate different PRRs in RPE cells, such as Toll-like, NOD-like and scavenger receptors along with complement system.
We also characterise the signalling pathways triggered by PRRs in evoking inflammatory responses. In addition, we will discuss
whether AMD pathology could represent the outcome of chronic activation of the innate immunity defence in human macula. 相似文献
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Dragoni Francesco Kaarniranta Kai 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2018,256(5):1031-1033
Graefe's Archive for Clinical and Experimental Ophthalmology - 相似文献
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Leena Pitkänen Petri Tommila Kai Kaarniranta Juha E Jääskeläinen Kati Kinnunen 《Acta ophthalmologica. Supplement》2014,92(2):101-104
Retinal arterial macroaneurysms are acquired saccular or fusiform dilatations of the large arterioles of the retina, usually within the first three orders of bifurcation. They are associated with systemic vascular conditions such as hypertension and arteriosclerotic disease occurring most commonly in elderly women. The primary reported symptom is a sudden loss of vision due to haemorrhage or oedema affecting the macula. Most of macroaneurysms regress without treatment and without causing decreased visual acuity. Poor visual outcome may occur secondary to foveal exudates and subfoveal haemorrhage. 相似文献
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Kai Kaarniranta 《Acta ophthalmologica. Supplement》2010,88(4):387-388
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Antero Salminen Anu Kauppinen Tiina Suuronen Kai Kaarniranta Johanna Ojala 《Journal of neuroinflammation》2009,6(1):41
The endoplasmic reticulum (ER) is involved in several crucial cellular functions, e.g. protein folding and quality control,
maintenance of Ca2+ balance, and cholesterol synthesis. Many genetic and environmental insults can disturb the function of ER and induce ER stress.
ER contains three branches of stress sensors, i.e. IRE1, PERK and ATF6 transducers, which recognize the misfolding of proteins
in ER and activate a complex signaling network to generate the unfolded protein response (UPR). Alzheimer's disease (AD) is
a progressive neurodegenerative disorder involving misfolding and aggregation of proteins in conjunction with prolonged cellular
stress, e.g. in redox regulation and Ca2+ homeostasis. Emerging evidence indicates that the UPR is activated in neurons but not in glial cells in AD brains. Neurons
display pPERK, peIF2α and pIRE1α immunostaining along with abundant diffuse staining of phosphorylated tau protein. Recent
studies have demonstrated that ER stress can also induce an inflammatory response via different UPR transducers. The most
potent pathways are IRE1-TRAF2, PERK-eIF2α, PERK-GSK-3, ATF6-CREBH, as well as inflammatory caspase-induced signaling pathways.
We will describe the mechanisms which could link the ER stress of neurons to the activation of the inflammatory response and
the evolution of pathological changes in AD. 相似文献
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Oxidative stress activates NLRP3 inflammasomes in ARPE-19 cells-Implications for age-related macular degeneration (AMD) 总被引:1,自引:0,他引:1
Kauppinen A Niskanen H Suuronen T Kinnunen K Salminen A Kaarniranta K 《Immunology letters》2012,147(1-2):29-33
Oxidative stress and inflammation are known to be associated with age-related macular degeneration (AMD). Retinal pigment epithelial (RPE) cells play the principal role in the immune defense of macula, and their dysfunction is a crucial event leading to clinically relevant changes seen in AMD. In the present study, we have examined the ability of oxidative stress to activate inflammasome signaling in the human ARPE-19 cells by adding the lipid peroxidation end product 4-hydroxynonenal (HNE) to cell cultures pre-treated or not treated with the endotoxin, LPS. Our results indicate that LPS and HNE significantly increased the production of IL-6 and IL-18, respectively. LPS treatment preceding HNE induced an even greater increase in the production of IL-18 than HNE alone. In addition to IL-18, HNE significantly increased the production of IL-1β. The productions of IL-1β and IL-18 were reduced in the cell cultures pre-treated with the Caspase-1 inhibitor. PCR analysis revealed that HNE induced an over 5-fold increase in the amount of NLRP3 mRNA compared to control cells; LPS had no effect. In conclusion, our present data suggest that oxidative stress can activate NLRP3 inflammasomes in RPE cells which occupy center stage in the pathogenesis of AMD. 相似文献