Anti-inflammatory property of quercetin through downregulation of ICAM-1 and MMP-9 in TNF-α-activated retinal pigment epithelial cells

Cytokine ◽  
2019 ◽  
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pp. 48-60 ◽  
Author(s):  
Shu-Chen Cheng ◽  
Yi-Hong Wu ◽  
Wen-Chung Huang ◽  
Jong-Hwei S. Pang ◽  
Tse-Hung Huang ◽  
...  
2019 ◽  
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pp. 175-182 ◽  
Author(s):  
Wojciech Garczorz ◽  
Enrique Gallego-Colon ◽  
Agnieszka Kosowska ◽  
Krzysztof Siemianowicz ◽  
Agnieszka Kłych-Ratuszny ◽  
...  

2015 ◽  
Vol 99 (5) ◽  
pp. 700-704 ◽  
Author(s):  
Nicoline M Korthagen ◽  
Kiki van Bilsen ◽  
Sigrid M A Swagemakers ◽  
Jeroen van de Peppel ◽  
Jeroen Bastiaans ◽  
...  

2012 ◽  
Vol 53 (4) ◽  
pp. 2208 ◽  
Author(s):  
Deeksha Gambhir ◽  
Sudha Ananth ◽  
Rajalakshmi Veeranan-Karmegam ◽  
Selvakumar Elangovan ◽  
Shanterian Hester ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1193
Author(s):  
Nayan Sanjiv ◽  
Pawarissara Osathanugrah ◽  
Emma Fraser ◽  
Tat Fong Ng ◽  
Andrew W. Taylor

A central characterization of retinal immunobiology is the prevention of proinflammatory activity by macrophages. The retinal pigment epithelial cells (RPEs) are a major source of soluble anti-inflammatory factors. This includes a soluble factor that induces macrophage apoptosis when the activity of the immunomodulating neuropeptide alpha-melanocyte-stimulating hormone (α-MSH) is neutralized. In this manuscript, isolated extracellular soluble membranes (ESMs) from primary RPE were assayed to see if they could be the soluble mediator of apoptosis. Our results demonstrated that RPE ESMs mediated the induction of macrophage apoptosis that was suppressed by α-MSH. In contrast, the RPE line ARPE-19, cultured under conditions that induce similar anti-inflammatory activity to primary RPEs, did not activate apoptosis in the macrophages. Moreover, only the ESMs from primary RPE cultures, and not those from the ARPE-19 cell cultures, expressed mFasL. The results demonstrate that RPE ESMs are a soluble mediator of apoptosis and that this may be a mechanism by which the RPEs select for the survival of α-MSH-induced suppressor cells.


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