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Updated: Jan 15, 2026
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Sympathetic Biomarker Dynamics Post-Myocardial Infarction: TH, PGP9.5, and SYN Expression Discordance in Murine
Tianshui Yu1, Baoqing Pei2, Dong Zhao1
1Key Laboratory of Evidence Science, China University of Political Science and Law, Ministry of Education, Beijing 100088, China.
Insights
This study identifies Tyrosine hydroxylase (TH) as the most specific biomarker for sympathetic nerve remodeling after myocardial infarction (MI). TH expression peaks at 7 days post-MI, offering insights into cardiac repair processes.
Area of Science:
- Cardiovascular Research
- Neuroscience
- Molecular Biology
Background:
- Myocardial infarction (MI) is a leading global cause of mortality.
- Sympathetic remodeling occurs post-MI, but its biomarker expression patterns are unclear.
- Tyrosine hydroxylase (TH), PGP9.5, and synaptophysin (SYN) are key sympathetic nerve markers.
Purpose of the Study:
- To characterize the temporal expression profiles of TH, PGP9.5, and SYN during sympathetic remodeling after MI.
- To determine the optimal biomarker for identifying sympathetic nerve changes post-MI.
Main Methods:
- MI was induced in C57BL/6 mice (n=60) via LAD ligation.
- Groups were analyzed at 2, 5, 7, and 10 days post-MI.
- Methods included histology (HE, Masson's trichrome), immunohistochemistry, and qRT-PCR for TH, PGP9.5, and SYN.
Main Results:
- TH, PGP9.5, and SYN were present in normal mouse cardiac sympathetic nerves.
- TH-positive sympathetic nerve proliferation occurred post-MI, peaking at 7 days.
- PGP9.5 localized to cardiomyocytes, and SYN to fibroblast-like cells in infarct zones; TH mRNA and protein peaked at 5-7 days.
Conclusions:
- TH is the most specific biomarker for post-MI sympathetic remodeling.
- PGP9.5 and SYN show ectopic expression in non-neuronal cells post-MI, requiring further study.
- Understanding these temporal biomarker changes aids in characterizing cardiac repair post-MI.
Abstract:
Myocardial infarction (MI) and its sequelae continue to be the leading cause of mortality globally. Following MI, a series of structural pathophysiological changes occur in the myocardium, including sympathetic remodeling. Tyrosine hydroxylase (TH), protein gene product 9.5 (PGP9.5), and synaptophysin (SYN) are recognized as key markers of sympathetic nerves. However, the expression patterns of these biomarkers during sympathetic remodeling, particularly their temporal profiles, remain insufficiently characterized. A cohort of 60 healthy adult male C57BL/6 mice was randomly divided into a control group (n = 12) and four MI groups with postoperative intervals of 2, 5, 7, and 10 days (n = 12/group). MI was induced via permanent ligation of the left anterior descending coronary artery (LAD). Cardiac tissues were subjected to histological analyses (HE and Masson's trichrome staining), immunohistochemical profiling, and quantitative reverse-transcriptase PCR (qRT-PCR) (TH, PGP9.5, and SYN). Immunohistochemical staining revealed that TH-, PGP9.5-, and SYN-immunopositive sympathetic nerves were present in the epicardium, myocardial interstitium, and the periphery of small blood vessels in normal mice. Normal cardiomyocytes were negative for TH but exhibited focal expression of PGP9.5 and SYN. In the myocardial infarction tissue, TH-positive staining indicated sympathetic nerve proliferation in the epicardium, myocardial infarction border zone, and infarct zone, with peak expression occurring at 7 days post-MI. In contrast to TH, PGP9.5 exhibited prominent immunoreactivity, specifically localized to the infarct core and peri-infarct zone cardiomyocytes, while SYN was primarily located in fibroblast-like cells within the same region. qRT-PCR analyses revealed that the time-dependent trends of TH, PGP9.5, and SYN mRNAs exhibited similarities, peaking between 5 and 7 days post-MI. TH demonstrates higher specificity than PGP9.5 and SYN in sympathetic nerve identification, solidifying its role as the optimal biomarker for post-MI sympathetic remodeling. The ectopic expression of PGP9.5 and SYN in non-neuronal cells within myocardial infarction tissue remains speculative and requires further mechanistic studies for validation.
