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Investigating Single‐cell Transcriptome Dynamics of the Dorsal Motor Nucleus of the Vagus (DMV) in a Rat Model of Remote Ischemic‐Reperfusion Cardioprotection (RIPC)
Author(s) -
Chong Weelic,
Balycheva Marina,
Schwaber James,
Vadigepalli Rajanikanth
Publication year - 2019
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.2019.33.1_supplement.742.3
Subject(s) - dorsal motor nucleus , cardioprotection , ischemic preconditioning , vagus nerve , myocardial infarction , medicine , neuroscience , pharmacology , anesthesia , biology , cardiology , ischemia , stimulation
The dorsal motor nucleus of the vagus (DMV) is one of the brainstem structures from which arises the vagus nerve, and is responsible for the vagal activity that protects the heart from reperfusion injury during an acute myocardial infarction. Remote ischemic‐reperfusion cardioprotection (RIPC) is a phenomenon known to protect the heart against injury via humoral and vagal mediation (Mastitskaya et al. 2012). It is hypothesized that RIPC cardioprotection may be mediated through changes in the gene expression of DMV neurons. However, the dynamics of gene expression in the DMV following RIPC is not known. Here, we performed RIPC by occluding the femoral artery, and using multiplex qPCR, we examined changes in gene expression of single cells taken from the DMV at several time points following RIPC. We conducted these experiments in both female and male rats and both left and right DMV. We also used a retrograde tracer to identify DMV neurons that travel to the heart and the gut, to identify different transcription profiles between these neuronal subpopulations. Our results show a distinct shift in transcriptomic identity of the neuronal subpopulations in the RIPC group over the sham controls. We conclude that there may be neuronal subpopulations in the DMV that are differentially activated following RIPC, which provides insights for translational applications of RIPC in decreasing reperfusion damage. Support or Funding Information We are supported by NIH NHLBI 5U01HL133360‐02 and NIH Director Office 3OT2OD023848. The funding sources played no role in study design, collection nor analysis of the data. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .