Increased expression of desmin and vimentin reduces bladder smooth muscle contractility via JNK2.

Bladder dysfunction is associated with the overexpression of the intermediate filament (IF) proteins desmin and vimentin in obstructed bladder smooth muscle (BSM). However, the mechanisms by which these proteins contribute to BSM dysfunction are not known. Previous studies have shown that desmin and vimentin directly participate in signal transduction.

Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.

Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE).

Altered detrusor contractility and voiding patterns in mice lacking the mechanosensitive TREK-1 channel.

Background: Previously published results from our laboratory identified a mechano-gated two-pore domain potassium channel, TREK-1, as a main mechanosensor in the smooth muscle of the human urinary bladder. One of the limitations of in vitro experiments on isolated human detrusor included inability to evaluate in vivo effects of TREK-1 on voiding function, as the channel is also expressed in the nervous system, and may modulate micturition via neural pathways. Therefore, in the present study, we aimed to assess the role of TREK-1 channel in bladder function and voiding patterns in vivo by using TREK-1 knockout (KO) mice.

Altered expression and modulation of the two-pore-domain (K) mechanogated potassium channel TREK-1 in overactive human detrusor.

Detrusor overactivity (DO) is the abnormal response of the urinary bladder to physiological stretch during the filling phase of the micturition cycle. The mechanisms of bladder smooth muscle compliance upon the wall stretch are poorly understood. We previously reported that the function of normal detrusor is regulated by TREK-1, a member of the mechanogated subfamily of two-pore-domain potassium (K) channels.

Regulation of urinary bladder function by protein kinase C in physiology and pathophysiology.

Background: Protein kinase C (PKC) is expressed in many tissues and organs including the urinary bladder, however, its role in bladder physiology and pathophysiology is still evolving. The aim of this review was to evaluate available evidence on the involvement of PKC in regulation of detrusor contractility, muscle tone of the bladder wall, spontaneous contractile activity and bladder function under physiological and pathophysiological conditions.

Methods: This is a non-systematic review of the published literature which summarizes the available animal and human data on the role of PKC signaling in the urinary bladder under different physiological and pathophysiological conditions.