Thrombin Regulates Chemokine Induction during Human Retinal Pigment Epithelial Cell/Monocyte Interaction

Yoshida, Ayako; Elner, Susan G.; Bian, Zhoufeng; Kunkel, Steven L.; Lukacs, Nicholas W.; Elner, Victor M.

doi:10.1016/s0002-9440(10)61793-2

Cited by 31 publications

(31 citation statements)

References 42 publications

(31 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, Corda et al (2001) showed that mitochondrial ROS generation induced by TNF-α may be inhibited by the ASMase inhibitor, desipramine and by the ceramide-activated protein kinase (CAPK) inhibitor, dimethylaminopurine (DMAP). Protein secretion of TNF-α, IL-β, or IFN-γ has not been demonstrated in RPE cells in vitro (Jaffe et al, 1992;Yoshida et al, 2001). However, descriptive studies of AMD lesions confirm the presence of macrophages expressing TNF-α and IL-1β (Oh et al, 1999), both of which we have shown to be potent inducers of RPE IL-8 and MCP-l (Elner et al, , 1997Bian et al, 2004).…”

Section: Discussionmentioning

confidence: 73%

Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

Yang

Elner

Bian

et al. 2007

Experimental Eye Research

Self Cite

347

242

View full text Add to dashboard Cite

Reactive oxygen species (ROS) generated during inflammation are believed to play critical roles in various ocular diseases. However, the underlying mechanisms remain poorly understood. We investigated if pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin-1β (IL-1β), and interferon-γ (IFN-γ), induce ROS in human retinal pigment epithelial (RPE) cells. TNF-α, IL-1β and IFN-γ increased both intracellular and extracellular ROS production in a time-and dosedependent manner. Thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial respiratory chain, blocked TNF-α-and IFN-γ-, but not IL-1β-induced ROS, whereas other two mitochondrial respiratory chain inhibitors, rotenone and antimycin A, had no effect. NADPH oxidase inhibitor (diphenylene iodinium) abolished the ROS production induced by IL-1β or IFN-γ, but not by TNF-α, whereas 6-aminonicotinamide (6AN), an inhibitor of the hexose monophosphate shunt (HMS), had no significant effects on the ROS induced by all three cytokines. ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-α, IL-1β and IFN-γ (P < 0.05). Collectively, these results demonstrate that TNF-α, IL-1β and IFN-γ increase mitochondrial-and NADPH oxidase-generated ROS in human RPE cells.

show abstract

Section: Discussionmentioning

confidence: 73%

Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

Yang

Elner

Bian

et al. 2007

Experimental Eye Research

Self Cite

347

242

View full text Add to dashboard Cite

show abstract

“…In an experimental baboon model, level of IL-6 and IL-8 peaked on day 2 after stasis-induced deep venous thrombosis and was associated with a venous inflammatory response consisting of early neutrophil infiltration into the vein wall, followed by extravasation of monocytes, macrophages, and lymphocytes. 27 Interestingly, Yoshida et al 28 reported that thrombin, a peptide whose main actions are related with clot formation (ie, converting fibrinogen to fibrin and activating platelet adhesion, aggregation, and secretion), induces secretion and mRNA expression of IL-8 and MCP-1 by HRPE cells. The inflammatory response elicited after a thrombotic event is needed for resolution of the thrombus.…”

Section: Il-8 and Mcp-1 In Brvo Macular Oedemamentioning

confidence: 99%

Vitreous levels of interleukine-8 and monocyte chemoattractant protein-1 in macular oedema with branch retinal vein occlusion

Fonollosa¹,

García-Arumí

Santos

et al. 2010

Eye

View full text Add to dashboard Cite

Purpose To investigate whether interleukine-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) are related with macular oedema in patients with branch retinal vein occlusions (BRVOs). Design Retrospective case-control study. Participants Nineteen patients who had macular oedema due to BRVO and nine patients with non-ischaemic ocular diseases (control group). Methods Macular oedema was examined by optical coherence tomography. Both venous blood and vitreous samples were obtained at the time of vitreoretinal surgery. IL-8 and MCP-1 levels in vitreous fluid and plasma were determined with enzyme-linked immunosorbent assay kits. Variables were compared with the Mann-Whitney U-test, Wilcoxon's signed-ranked test, and the v 2 -test, when appropriate. To examine correlations, Spearman's rank-order correlation coefficients were calculated. Statistical significance was set at Po0.05. Results The vitreous fluid levels of IL-8 (median: 63.5 pg/ml) and MCP-1 (median: 1522.4 pg/ml) were significantly higher in the patients with BRVO than in the control group (median: 5.1 and 746.5 pg/ml respectively; Po0.001 and o0.001 respectively). Vitreous IL-8 and MCP-1 were significantly correlated in patients with BRVO (P ¼ 0.009). Conclusions Both IL-8 and MCP-1 were elevated in the vitreous fluid of patients with BRVO and macular oedema. Both chemokines may contribute to the pathogenesis of macular oedema in patients with BRVO.

show abstract

“…Direct cell-to-cell contact has also been shown to influence cellular response, function, and survival in many kinds of cell types (Meszaros et al, 2000;Seshiah et al, 2002;Yoshida et al, 2001a). HRPE cells are frequently associated with monocytes in PVR, ARMD, and uveitis (Baudouin et al, 1992;Chan et al, 1985;Harper et al, 1992;Jerdan et al, 1989;Kampik et al, 1981;Vinores et al, 1990).…”

mentioning

confidence: 99%

Activated Monocytes Induce Human Retinal Pigment Epithelial Cell Apoptosis Through Caspase-3 Activation

Yoshida

Elner

Bian

et al. 2003

Laboratory Investigation

Self Cite

View full text Add to dashboard Cite

Michigan SUMMARY:Dysfunction and loss of human retinal pigment epithelial (HRPE) cells is a significant component of many ocular diseases, in which mononuclear phagocyte infiltration at the HRPE-related interface is also observed. In this study, we investigated whether HRPE cell apoptosis may be induced by overlay of IFN-␥-activated monocytes. Human monocytes primed with IFN-␥ overlaid directly onto HRPE cells elicited significant increases in terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive HRPE cells (p Ͻ 0.0001) and decreases of proliferating cell nuclear antigen-positive (p Ͻ 0.0001) HRPE cells. The activated monocytes also induced HRPE cell caspase-3 activation, which was inhibited by the caspase-3 inhibitor, Z-DEVD-fmk. However, co-incubations in which activated monocytes were prevented from direct contact with HRPE cells or in which the monocytes were separated from the HRPE cells after 30 minutes of direct contact, did not induce significant HRPE cell apoptosis. Function-blocking anti-CD18 and anti-intercellular adhesion molecule-1 (ICAM-1) antibodies significantly reduced activated monocyte-induced TUNEL-positive HRPE cells by 48% (p ϭ 0.0051) and 38% (p ϭ 0.046), respectively. Anti-CD18 and anti-ICAM-1 antibodies significantly inhibited caspase-3 activity by 56% (p Ͻ 0.0001) and 45% (p Ͻ 0.0001), respectively. However, antibodies to vascular cell adhesion molecule-1, TNF-␣, IL-1␤, or TNF-related apoptosisinducing ligand did not inhibit apoptosis or caspase-3 activation. Direct overlay of monocytes also induced reactive oxygen metabolites (ROM) within HRPE cells. The intracellular HRPE cell ROM production was inhibited by the anti-CD18 and anti-ICAM-1 antibodies, but not by superoxide dismutase, presumably due to its failure to penetrate into HRPE cells. Accordingly, neither superoxide dismutase nor N G -monomethyl-L-arginine had significant effects on HRPE cell apoptosis or caspase-3 activation. Our results suggest that activated monocytes may induce ROM in HRPE cells through cell-to-cell contact, in part via CD18 and ICAM-1, and promote HRPE cell apoptosis. These mechanisms may compromise HRPE cell function and survival in a variety of retinal diseases. (Lab Invest 2003, 83:1117-1129.

show abstract

Thrombin Regulates Chemokine Induction during Human Retinal Pigment Epithelial Cell/Monocyte Interaction

Cited by 31 publications

References 42 publications

Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

Vitreous levels of interleukine-8 and monocyte chemoattractant protein-1 in macular oedema with branch retinal vein occlusion

Activated Monocytes Induce Human Retinal Pigment Epithelial Cell Apoptosis Through Caspase-3 Activation

Contact Info

Product

Resources

About