Proteomics

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Multiplexed quantitative proteomics in an autoimmune mice model of myocarditis (EAM)

ABSTRACT: We performed a high-throughput, multiplexed quantitative proteomics analysis to determine protein abundance changes produced by BML-111 treatment in EAM and Ctrl mice. EAM was induced in 7 weeks-old BALB/c female mice by immunization at days 0 and 7 with a subcutaneous injection of 350 μg of murine cardiac myosin (MyHCα) in a 1:1 emulsion with complete Freund’s Adjuvant (SIGMA). MyHCα was isolated from hearts of Balb/c mice; control mice were injected with a 1:1 emulsion of physiological saline solution with complete Freund’s Adjuvant. Mice were treated daily for two weeks from day 7 by intraperitoneal injection with two complementary treatments: 1mg/Kg BML-111(Enzo Life Science) or its vehicle (2.5% ethanol). The proteomics analysis was performed in heart tissue protein extracts (four animals per group: Ctrl+Veh, EAM+Veh, Ctrl+BML and EAM+BML.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Inmaculada Jorge  

LAB HEAD: Jesús María Vázquez Cobos

PROVIDER: PXD024345 | Pride | 2022-12-07

REPOSITORIES: Pride

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IJ_Lisardo_TMT1_1.msf Msf
IJ_Lisardo_TMT1_1.raw Raw
IJ_Lisardo_TMT1_2.msf Msf
IJ_Lisardo_TMT1_2.raw Raw
IJ_Lisardo_TMT1_3.msf Msf
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Publications

Specialized proresolving mediators and, in particular, 5(S), (6)R, 7-trihydroxyheptanoic acid methyl ester (BML-111) emerge as new therapeutic tools to prevent cardiac dysfunction and deleterious cardiac damage associated with myocarditis progression. The cardioprotective role of BML-111 is mainly caused by the prevention of increased oxidative stress and nuclear factor erythroid-derived 2-like 2 (NRF2) down-regulation induced by myocarditis. At the molecular level, BML-111 activates NRF2 signal  ...[more]

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