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Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization

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Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization. / Malsy, Jakob; Alvarado, Andrea C; Lamontagne, Joseph O; Strittmatter, Karin; Marneros, Alexander G.

in: ELIFE, Jahrgang 9, 11.12.2020.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Malsy, J, Alvarado, AC, Lamontagne, JO, Strittmatter, K & Marneros, AG 2020, 'Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization', ELIFE, Jg. 9. https://doi.org/10.7554/eLife.60194

APA

Malsy, J., Alvarado, A. C., Lamontagne, J. O., Strittmatter, K., & Marneros, A. G. (2020). Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization. ELIFE, 9. https://doi.org/10.7554/eLife.60194

Vancouver

Malsy J, Alvarado AC, Lamontagne JO, Strittmatter K, Marneros AG. Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization. ELIFE. 2020 Dez 11;9. https://doi.org/10.7554/eLife.60194

Bibtex

@article{c377921a76994a9d8320f2579832b1b0,
title = "Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization",
abstract = "NLRP3 inflammasome activation and complement-mediated inflammation have been implicated in promoting choroidal neovascularization (CNV) in age-related macular degeneration (AMD), but central questions regarding their contributions to AMD pathogenesis remain unanswered. Key open questions are (1) whether NLRP3 inflammasome activation mainly in retinal pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whether inflammasome activation in CNV occurs via NLRP3 or also through NLRP3-independent mechanisms, and (3) whether complement activation induces inflammasome activation in CNV. Here we show in a neovascular AMD mouse model that NLRP3 inflammasome activation in non-RPE cells but not in RPE cells promotes CNV. We demonstrate that both NLRP3-dependent and NLRP3-independent inflammasome activation mechanisms induce CNV. Finally, we find that complement and inflammasomes promote CNV through independent mechanisms. Our findings uncover an unexpected role of non-NLRP3 inflammasomes for CNV and suggest that combination therapies targeting inflammasomes and complement may offer synergistic benefits to inhibit CNV.",
author = "Jakob Malsy and Alvarado, {Andrea C} and Lamontagne, {Joseph O} and Karin Strittmatter and Marneros, {Alexander G}",
note = "{\textcopyright} 2020, Malsy et al.",
year = "2020",
month = dec,
day = "11",
doi = "10.7554/eLife.60194",
language = "English",
volume = "9",
journal = "ELIFE",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - Distinct effects of complement and of NLRP3- and non-NLRP3 inflammasomes for choroidal neovascularization

AU - Malsy, Jakob

AU - Alvarado, Andrea C

AU - Lamontagne, Joseph O

AU - Strittmatter, Karin

AU - Marneros, Alexander G

N1 - © 2020, Malsy et al.

PY - 2020/12/11

Y1 - 2020/12/11

N2 - NLRP3 inflammasome activation and complement-mediated inflammation have been implicated in promoting choroidal neovascularization (CNV) in age-related macular degeneration (AMD), but central questions regarding their contributions to AMD pathogenesis remain unanswered. Key open questions are (1) whether NLRP3 inflammasome activation mainly in retinal pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whether inflammasome activation in CNV occurs via NLRP3 or also through NLRP3-independent mechanisms, and (3) whether complement activation induces inflammasome activation in CNV. Here we show in a neovascular AMD mouse model that NLRP3 inflammasome activation in non-RPE cells but not in RPE cells promotes CNV. We demonstrate that both NLRP3-dependent and NLRP3-independent inflammasome activation mechanisms induce CNV. Finally, we find that complement and inflammasomes promote CNV through independent mechanisms. Our findings uncover an unexpected role of non-NLRP3 inflammasomes for CNV and suggest that combination therapies targeting inflammasomes and complement may offer synergistic benefits to inhibit CNV.

AB - NLRP3 inflammasome activation and complement-mediated inflammation have been implicated in promoting choroidal neovascularization (CNV) in age-related macular degeneration (AMD), but central questions regarding their contributions to AMD pathogenesis remain unanswered. Key open questions are (1) whether NLRP3 inflammasome activation mainly in retinal pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whether inflammasome activation in CNV occurs via NLRP3 or also through NLRP3-independent mechanisms, and (3) whether complement activation induces inflammasome activation in CNV. Here we show in a neovascular AMD mouse model that NLRP3 inflammasome activation in non-RPE cells but not in RPE cells promotes CNV. We demonstrate that both NLRP3-dependent and NLRP3-independent inflammasome activation mechanisms induce CNV. Finally, we find that complement and inflammasomes promote CNV through independent mechanisms. Our findings uncover an unexpected role of non-NLRP3 inflammasomes for CNV and suggest that combination therapies targeting inflammasomes and complement may offer synergistic benefits to inhibit CNV.

U2 - 10.7554/eLife.60194

DO - 10.7554/eLife.60194

M3 - SCORING: Journal article

C2 - 33305736

VL - 9

JO - ELIFE

JF - ELIFE

SN - 2050-084X

ER -