{'fraction_non_alphanumeric': 0.04341926729986431, 'fraction_numerical': 0.03188602442333786, 'mean_word_length': 5.413043478260869, 'pattern_counts': {'":': 0, '<': 1, '<?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}}
A2B adenosine receptors promote retention of cardiac stem cells in a myofibroblast‐like state induced by myocardial infarction (652.11)

Adult cardiac stem cells can contribute to scar formation by acquiring myofibroblast phenotype in response to myocardial injury. Adenosine levels increase in ischemic hearts and modulate cardiac cell functions via binding to adenosine receptors (AR). Here, we tested the hypothesis that A2BAR regulate a reversible transition of cardiac Sca1+CD31‐ mesenchymal stem cells into a myofibroblast‐like state in a mouse model of myocardial infarction (MI). Using flow cytometry, we found that MI resulted in a rapid increase in the numbers of alpha smooth muscle actin (αSMA)‐positive Sca‐1+CD31‐ cells by day 5, followed by gradual decline. Genetic ablation of A2BAR had no effect on accumulation of αSMA‐positive Sca‐1+CD31‐ cells. However, their numbers remained significantly higher in wild‐type (WT) compared with A2BAR knockout (KO) hearts during their deactivation (by 1.2 and 2‐fold on post‐MI days 7 and 14, respectively; p<0.05) indicating that this process is modulated by A2BAR signaling. Furthermore, the numbers of αSMA/collagen I double positive Sca‐1+CD31‐ cells remained higher in WT compared with A2BAR KO hearts by 73%±10% and 54%±6% on post‐MI days 7 and 14, respectively. Our data suggest that A2BAR signaling can play a role in scar evolution by promoting retention of Sca‐1+CD31‐ cells in their myofibroblast‐like state.