Josiah Brown Poster Abstract


Aubrey J. Walker
Reza Ardehali MD, PhD
Ngoc Nguyen, Peng Zhao, Shuin Park, Lizhu Chen, Hong Zhu
Analysis of Neonatal-Plasma-Derived Proteins Mediating Cardioprotective Effects After Ischemia-Reperfusion Injury

Ischemic heart disease, including acute myocardial infarction (MI), is a leading cause of morbidity and mortality in the United States, with disproportionate impact on minority, correctional and aging populations.[1],[2]

Age-related changes and degeneration are important risk factors for ischemic heart disease and directly increase the risk of future acute myocardial infarction (MI), ischemic heart morbidity and other cardiovascular sequalae.[3]

In conjunction with thrombolytic treatment, the standard of therapy employed to reduce ischemic injury secondary to MI has long consisted of immediate primary percutaneous coronary intervention (PPCI).[4]

However, the process of PPCI itself can induce irreversible cardiomyocyte death, termed ischemia-reperfusion (I/R) injury, for which there are currently no effective therapies.[5]

Our lab has compelling evidence demonstrating a protective effect of neonatal murine plasma on cardiac function, scar formation, and vascular density after myocardial injury.

To examine the specific mechanism by which factor(s) in young blood offers protection from myocardial damage, we first sought to analyze and compare the proteomes of neonatal and aged mouse plasma to identify the top upregulated and downregulated proteins that might account for the improvements in cardiac function and remodeling following ischemia-reperfusion injury.

Analysis of the top 100 upregulated proteins in neonatal plasma identified key biological processes of translation and peptide catabolism, with ribosomal-associated proteins as potential factors involved in the cardioprotective effects observed.

Further studies to confirm the proteomic data as well as biological validation of top candidates are needed to identify potentially novel therapeutics to prevent the progression to heart failure after an acute myocardial infarction.

Given the growing social and financial burden of cardiovascular disease, the relative stagnation of therapeutic discoveries for MI management and this disease’s disproportionate effects on minority, correctional, and aging populations, further research investigating the underlying cardioprotective mechanisms of neonatal plasma represents a moral, economic and scientific imperative.