{'fraction_non_alphanumeric': 0.023045267489711935, 'fraction_numerical': 0.00411522633744856, 'mean_word_length': 5.108040201005025, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Abstract 323: Gamma-Enolase in Adult Cardiac Myocytes: A Study of Subcellular Localization and Post-Myocardial Infarction Modulation


 Background:
 Gamma-enolase, or neuron-specific enolase, is a multifunctional protein which is primarily found in neurons and neuroendocrine cells. Although the main role of gamma-enolase is associated with enzymatic activity during aerobic glycolysis, recently, it has been implicated in a variety of pathophysiological processes including inflammation, extracellular matrix degradation and cell survival after ischemic insult. Over the last decades, there have been a number of reports demonstrating the expression of gamma-enolase in the heart. Surprisingly, the latter finding has not received much attention in the past. Considering that this protein can play an important role in cellular adaptation to the ischemic environment we decided to examine the expression of gamma-enolase in the heart at different time points following a myocardial infarction (MI).
 
 
 Methods:
 A transmural MI was induced in male, middle-aged Sprague-Dawley rats by permanent left coronary artery ligation. The rats were euthanized 3 days, 1, 2, 4 and 8 weeks after MI and their hearts were processed into paraffin for immunostaining and quantitative morphometry.
 
 
 Results:
 We found that in post-MI heart gamma-enolase protein was expressed in cardiac myocytes of the remote myocardium as well as in the muscle cells surviving inside the transmural scar. On a subcellular level, the gamma-enolase expression overlapped with the I-bands of the sarcomeres. Despite the heterogeneity of the gamma-enolase fluorescence intensity among individual cardiac myocytes, there was no evident correlation between the size of the cells and the intensity of the gamma-enolase immunofluorescence in any region of the post-MI heart, although the immunofluorescence intensity of gamma-enolase in myocytes of the remote myocardium was always greater than that in myocytes surviving within the transmural scar. Most importantly, we determined that the intensity of gamma-enolase immunofluorescence recorded in cardiac myocytes has experienced an evident stepwise reduction at 1 and 8 weeks following MI.
 
 
 Conclusions:
 Taken together, our findings reveal that the cardiac myocytes of the adult rat heart express gamma-enolase and that the expression of this protein has been altered during post-MI cardiac remodeling.
