{'fraction_non_alphanumeric': 0.03930530164533821, 'fraction_numerical': 0.0009140767824497258, 'mean_word_length': 4.951086956521739, '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}}
Nonselective alpha-/beta- AR antagonists can inhibit pericyte proliferation, migration, and secretion in vitro.

It has been reported that the beta-adrenergic receptor blocker (propranolol) and the a-adrenergic receptor (AR) blocker (phentolamine) both can inhibit human endothelial cell (EC) angiogenesis in vitro. However, it is unknown whether this inhibition also acts on pericytes. The present study aimed to determine how pericytes react to treatment with an a-/β-AR blocker. In the study, cell proliferation assays and scratch assay were performed to assess the effect of phentolamine or propranolol on cell proliferation and migration. Western blot and ELISA were employed to determine changes in VEGF-A and Ang-1 expression levels. The results indicated that the nonselective a-/β- AR blocker inhibited the proliferation, migration, and secretion of pericytes. The use of the nonselective a-/β- AR blocker might have an impact on vascularization and vascular maturation. Our research suggests the rational use of nonselective a-/β- AR blockers to treat angiogenesis-dependent diseases.