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Transcriptomic Analysis of the Stellate Ganglion After MI
Author(s) -
Bayles Richard,
Olivas Antoinette,
Gardner Ryan,
Burchard Julja,
Habecker Beth
Publication year - 2017
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.31.1_supplement.1071.5
Subject(s) - transcriptome , stellate ganglion , hepatic stellate cell , myocardial infarction , gene expression , rna , glutamate receptor , biology , gene , medicine , cardiology , receptor , pathology , genetics , alternative medicine
Survivors of a myocardial infarction (MI) remain at serious risk of sudden cardiac death due to lethal arrhythmias. It is known from studies in humans and dogs that electrical and structural remodeling of the stellate sympathetic neurons occurs following MI, including an increase in size and excitability. Increased excitability may be due to a variety of sources including increased dendritic field size, more synaptic inputs or altered ion channel expression to name a few. In an effort to identify neuronal genes regulated by MI, we have performed RNA sequencing (RNAseq) of RNA extracted from the stellate ganglia of mice 14 days after MI or sham surgery. Infarction was induced by 45 min occlusion of the left anterior descending coronary (LAD) artery, and sham operated animals underwent the same procedure with no occlusion. After 14 days, left ventricular scar tissue was visible in the occluded animals, and gene expression changes in the infarct and borderzone were in agreement with previous studies of MI. Library preparation was completed using the TruSeq Stranded Total RNA kit (Illumina), and sequencing using the Illumina HiSeq 2500 Sequencer. Sequence alignment and QC was performed using STAR. RNA expression across all samples was highly consistent, however small yet consistent changes in the expression of genes were detected between mice with MI and controls. These changes included genes encoding ion channels, receptors, synaptic proteins and actin remodeling proteins. Support or Funding Information This work was supported by NIH RO1 HL093056