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Label‐free proteomic analysis uncovers early molecular link to abnormal cardiac neurotransmission in pro‐hypertension rats (856.2)
Author(s) -
Burton RebeccaAnn,
Schmidt Carla,
Lu ChiehJu,
Larsen Hege,
Gallone Giuseppe,
Li Dan,
Hao Guoliang,
Nikiforova Natalia,
Bub Gil,
Kramer Holger,
Robinson Carol,
Paterson David
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.856.2
Subject(s) - proteomics , neuroscience , microbiology and biotechnology , endocrinology , disease , medicine , biology , bioinformatics , chemistry , gene , biochemistry
Sympathetic hyper‐responsiveness is an early hallmark of hypertension and has been linked to early metabolic and oxidative stress. We used label‐free quantitative proteomics to compare cardiac sympathetic neurons from the neonatal pro‐hypertensive rat (SHR) with neurons from an age matched normotensive control (WKY). Canonical protein interaction pathways and networks were generated using Ingenuity Pathway Analysis (IPA) to study protein regulation. We also performed functional association network analysis using STRING and the Girvan‐Newman fast greedy algorithm to produce protein clusters. Marked differences in proteins coupled to calcium signalling, metabolic processes, tissue architecture and cell migration were seen in the diseased neurons. In particular, we found abnormally high levels of non‐muscle myosin 9 in SHR neurons. This protein has been implicated in cytokinesis, vesicular trafficking, neurotransmitter release and familial human cardiovascular and neurological disease. Our findings indicate that direct modulation of myosin 9 could present a novel therapeutic target to manage abnormal sympathetic activation. Grant Funding Source : British Heart Foundation