Washington, August 8 (ANI): Japanese researchers have uncovered a molecular mechanism that enables bladder urothelial cells to feel stretch stimulation, and thereby sense fullness of urine.
Prof. Makoto Tominaga and Dr. Takaaki Sokabe, of the National Institute for Physiological Sciences (NIPS), and Prof. Masayuki Takeda, Dr. Isao Araki and Dr. Tsutomu Mochizuki, of Yamanashi University, say that bladder is known to release ATP that activates micturition reflex pathway during urine storage.
However, they add, it has been unknown how urothelial cells sense bladder distension.
The researchers have revealed that they examined the function of 'TRPV4' protein abundantly expressed in urothelial cells.
They developed a special apparatus to measure cell responses upon stretch stimulation, which mimics bladder distension.
The team observed that upon stretch stimulation, robust Ca2+ influx and following ATP release were observed in urothelial cells.
The researchers said that those phenomena were almost completely attributed to TRPV4 activation, since such responses were eliminated by a TRPV4 inhibitor and reduced in TRPV4-deficient urothelial cells.
Dr. Sokabe said: "This is the first report to show that TRPV4 is a primal stretch-detector in urothelial cells. Given that TRPV4 is critically involved in the sensing mechanism in the bladder, development of chemicals modulating TRPV4 activity may be useful for treatment of bladder disorders such as overactive bladder and pollakiuria."
The study has been reported in the Journal of Biological Chemistry. (ANI)
Prof. Makoto Tominaga and Dr. Takaaki Sokabe, of the National Institute for Physiological Sciences (NIPS), and Prof. Masayuki Takeda, Dr. Isao Araki and Dr. Tsutomu Mochizuki, of Yamanashi University, say that bladder is known to release ATP that activates micturition reflex pathway during urine storage.
However, they add, it has been unknown how urothelial cells sense bladder distension.
The researchers have revealed that they examined the function of 'TRPV4' protein abundantly expressed in urothelial cells.
They developed a special apparatus to measure cell responses upon stretch stimulation, which mimics bladder distension.
The team observed that upon stretch stimulation, robust Ca2+ influx and following ATP release were observed in urothelial cells.
The researchers said that those phenomena were almost completely attributed to TRPV4 activation, since such responses were eliminated by a TRPV4 inhibitor and reduced in TRPV4-deficient urothelial cells.
Dr. Sokabe said: "This is the first report to show that TRPV4 is a primal stretch-detector in urothelial cells. Given that TRPV4 is critically involved in the sensing mechanism in the bladder, development of chemicals modulating TRPV4 activity may be useful for treatment of bladder disorders such as overactive bladder and pollakiuria."
The study has been reported in the Journal of Biological Chemistry. (ANI)
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