{'fraction_non_alphanumeric': 0.025727826675693975, 'fraction_numerical': 0.012863913337846988, 'mean_word_length': 6.038095238095238, '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}}
Novel insight into human urinary bladder function: the role of transient receptor potential melastatin 4 channels (865.6)

Transient receptor potential melastatin 4 (TRPM4) channels have been recently identified in urinary bladder smooth muscle (UBSM) in rodents. Here, we applied a combined experimental approach to study the role of TRPM4 channels in human UBSM function. We used RT‐PCR, Western blot, immunohistochemistry, immunocytochemistry, patch‐clamp electrophysiology, and isometric tension recordings of human UBSM isolated strips from donor patients. mRNA message for TRPM4 channels in whole tissue and single UBSM cells was detected. Western blot and immunohistochemistry revealed TRPM4 protein expression in whole UBSM tissue. Immunocytochemistry further confirmed TRPM4 protein expression in DSM single cells. Voltage‐clamp experiments showed that the TRPM4 channel inhibitor 9‐phenanthrol decreased the transient inward cation currents (TICCs) recorded at ‐70 mV. Inhibition of IP3‐receptors with xestospongin‐C also abolished the TICCs activity in human UBSM. 9‐phenanthrol hyperpolarized the UBSM membrane potential and attenuated the spontaneous phasic, carbachol‐induced and nerve‐evoked contractions in UBSM isolated strips. The results reveal that TRPM4 channels are present in human UBSM and are critical regulators of human UBSM excitability and contractility. UBSM TRPM4 channels should be considered further as new targets overactive bladder treatment.