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Published on: June 11, 2020
Altered norepinephrine content and ventricular function in p75NTR-/- mice after myocardial infarction
Christina U Lorentz1, William R Woodward, Kevin Tharp
1Department of Physiology, Oregon Health & Science University, Portland, OR 97239, USA.
Autonomic Neuroscience : Basic & Clinical
|June 8, 2011
Summary
Mice lacking p75 neurotrophin receptor (p75NTR) showed no improved cardiac function after myocardial infarction. This study investigated nerve growth factor signaling in post-infarct sympathetic remodeling.
Area of Science:
- Cardiovascular Biology
- Neuroscience
- Molecular Biology
Background:
- Cardiac sympathetic neurons regulate heart function via norepinephrine release.
- Nerve growth factor (NGF) signaling, through TrkA and p75NTR, influences sympathetic transmission and post-infarct remodeling.
- p75NTR plays a role in modulating NGF's effects on the sympathetic nervous system.
Purpose of the Study:
- To investigate the impact of lacking p75 neurotrophin receptor (p75NTR) on cardiac sympathetic neuropeptide expression, norepinephrine levels, and ventricular function following myocardial infarction (MI).
- To understand the role of p75NTR in nerve growth factor (NGF) signaling in the context of cardiac injury and repair.
Main Methods:
- Utilized p75NTR knockout (p75NTR-/-) and wildtype (WT) mice subjected to ischemia-reperfusion surgery to induce myocardial infarction.
- Assessed infarct size, cardiac sympathetic neuropeptide mRNA expression (VIP, galanin, PACAP), TrkA receptor expression, and norepinephrine content.
- Measured left ventricular pressure and contractility (dP/dt(MAX), dP/dt(MIN)) at 3 and 7 days post-MI, with and without pharmacological stimulation.
Main Results:
- Infarct size and neuropeptide/TrkA expression were similar between p75NTR-/- and WT mice.
- Elevated norepinephrine content was observed in the base of p75NTR-/- ventricles, but not below the occlusion site.
- Ventricular pressure and dP/dt(MAX) were significantly lower in p75NTR-/- hearts compared to WT hearts 7 days post-MI, indicating impaired cardiac function.
Conclusions:
- The absence of p75NTR did not confer protection or enhance cardiac function after myocardial infarction.
- Altered NGF signaling through p75NTR does not appear to improve ventricular function or sympathetic remodeling in the post-infarct heart.
- These findings suggest p75NTR is not a therapeutic target for improving outcomes after myocardial infarction.
