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      The Expression and Function of Piezo Channels in Bladder

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          Abstract

          The ability for bladder to perceive and analyze mechanical stimuli, such as stretch and filling, is crucial for its functions, such as urinary storage and voiding. The Piezo channel family, including Piezo1 and Piezo2, represents one of the most essential mechanosensitive ion channels in mammals and is involved in a wide array of physiological and pathological processes. It has been demonstrated in numerous investigations that Piezo channels play a key role in mechanical transduction in various types of cells in bladder by converting mechanical stimuli into biological signals. Notably, mounting evidence suggests that Piezo channels are functionally significant for bladder and are related to several bladder disorders. This review systematically summarizes the importance/role and features of Piezo channels in bladder, including their biophysical properties, location, and functions, with attention specifically paid to their association with the physiology and pathophysiology of bladder. This review aims to provide a novel perspective for the future clinical treatment of bladder dysfunction.

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          Most cited references64

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          Mechanical stretch triggers rapid epithelial cell division through Piezo1

          SA Gudipaty, J Lindblom, PD Loftus … (2017)
          Despite acting as a barrier for the organs they encase, epithelial cells turnover at some of the fastest rates in the body. Yet, epithelial cell division must be tightly linked to cell death to preserve barrier function and prevent tumour formation. How do the number of dying cells match those dividing to maintain constant numbers? We previously found that when epithelial cells become too crowded, they activate the stretch-activated channel Piezo1 to trigger extrusion of cells that later die 1 . Conversely, what controls epithelial cell division to balance cell death at steady state? Here, we find that cell division occurs in regions of low cell density, where epithelial cells are stretched. By experimentally stretching epithelia, we find that mechanical stretch itself rapidly stimulates cell division through activation of the same Piezo1 channel. To do so, stretch triggers cells paused in early G2 to activate calcium-dependent ERK1/2 phosphorylation that activates cyclin B transcription necessary to drive cells into mitosis. Although both epithelial cell division and cell extrusion require Piezo1 at steady state, the type of mechanical force controls the outcome: stretch induces cell division whereas crowding induces extrusion. How Piezo1-dependent calcium transients activate two opposing processes may depend on where and how Piezo1 is activated since it accumulates in different subcellular sites with increasing cell density. In sparse epithelial regions where cells divide, Piezo1 localizes to the plasma membrane and cytoplasm whereas in dense regions where cells extrude, it forms large cytoplasmic aggregates. Because Piezo1 senses both mechanical crowding and stretch, it may act as a homeostatic sensor to control epithelial cell numbers, triggering extrusion/apoptosis in crowded regions and cell division in sparse regions.
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            Endothelial cation channel PIEZO1 controls blood pressure by mediating flow-induced ATP release.

            ShengPeng Wang, Ramesh Chennupati, Harmandeep Kaur … (2016)
            Arterial blood pressure is controlled by vasodilatory factors such as nitric oxide (NO) that are released from the endothelium under the influence of fluid shear stress exerted by flowing blood. Flow-induced endothelial release of ATP and subsequent activation of Gq/G11-coupled purinergic P2Y2 receptors have been shown to mediate fluid shear stress-induced stimulation of NO formation. However, the mechanism by which fluid shear stress initiates these processes is unclear. Here, we have shown that the endothelial mechanosensitive cation channel PIEZO1 is required for flow-induced ATP release and subsequent P2Y2/Gq/G11-mediated activation of downstream signaling that results in phosphorylation and activation of AKT and endothelial NOS. We also demonstrated that PIEZO1-dependent ATP release is mediated in part by pannexin channels. The PIEZO1 activator Yoda1 mimicked the effect of fluid shear stress on endothelial cells and induced vasorelaxation in a PIEZO1-dependent manner. Furthermore, mice with induced endothelium-specific PIEZO1 deficiency lost the ability to induce NO formation and vasodilation in response to flow and consequently developed hypertension. Together, our data demonstrate that PIEZO1 is required for the regulation of NO formation, vascular tone, and blood pressure.
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              Piezo2 is the major transducer of mechanical forces for touch sensation in mice.

              Sanjeev S Ranade, Seung-Hyun Woo, Adrienne Dubin … (2014)
              The sense of touch provides critical information about our physical environment by transforming mechanical energy into electrical signals. It is postulated that mechanically activated cation channels initiate touch sensation, but the identity of these molecules in mammals has been elusive. Piezo2 is a rapidly adapting, mechanically activated ion channel expressed in a subset of sensory neurons of the dorsal root ganglion and in cutaneous mechanoreceptors known as Merkel-cell-neurite complexes. It has been demonstrated that Merkel cells have a role in vertebrate mechanosensation using Piezo2, particularly in shaping the type of current sent by the innervating sensory neuron; however, major aspects of touch sensation remain intact without Merkel cell activity. Here we show that mice lacking Piezo2 in both adult sensory neurons and Merkel cells exhibit a profound loss of touch sensation. We precisely localize Piezo2 to the peripheral endings of a broad range of low-threshold mechanoreceptors that innervate both hairy and glabrous skin. Most rapidly adapting, mechanically activated currents in dorsal root ganglion neuronal cultures are absent in Piezo2 conditional knockout mice, and ex vivo skin nerve preparation studies show that the mechanosensitivity of low-threshold mechanoreceptors strongly depends on Piezo2. This cellular phenotype correlates with an unprecedented behavioural phenotype: an almost complete deficit in light-touch sensation in multiple behavioural assays, without affecting other somatosensory functions. Our results highlight that a single ion channel that displays rapidly adapting, mechanically activated currents in vitro is responsible for the mechanosensitivity of most low-threshold mechanoreceptor subtypes involved in innocuous touch sensation. Notably, we find that touch and pain sensation are separable, suggesting that as-yet-unknown mechanically activated ion channel(s) must account for noxious (painful) mechanosensation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Bladder (San Franc)
                Journal ID (iso-abbrev): Bladder (San Franc)
                Title: Bladder
                Publisher: Bladder
                ISSN (Electronic): 2327-2120
                Publication date Collection: 2023
                Publication date (Electronic): 30 October 2023
                Volume: 10
                Electronic Location Identifier: e21200008
                Affiliations
                [1 ]Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan 430030, Hubei, China
                [2 ]Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan 430030, Hubei, China
                Author notes
                *Corresponding author: Zhong Chen, Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China. Email 1991tj0590@ 123456hust.edu.cn

                Conflict of interest: No conflict of interest was declared by the authors.

                Abbreviation used: [Ca 2+]i, Intracellular calcium concentration; ATP, Adenosine triphosphate; BOO, Bladder outlet obstruction; CYP-induced, Cyclophosphamide-induced; DCP, Diabetic cystopathy; DRG, Dorsal root ganglia; FISH, Fluorescence in situ hybridization; GsMTx4, Grammostola spatulate mechanotoxin 4; ICCs, Interstitial Cajal-like cells; ICs, Interstitial cells; KO, Knockout; LP, Lamina propria ; LP-ICs, Interstitial cells in bladder lamina propria; LUT, Lower urinary tract; LUTS, Lower urinary tract symptoms; NCX1, Na +/Ca 2+ exchanger 1; OAB, Overactive bladder; pBOO, Partial bladder outlet obstruction; PIEZO1-tdT, PIEZO1 fused to the red fluorescent reporter tandem-dimer Tomato; SAC, Stretch-activated ion channel ; SACs, Stretch-activated ion channels; TRPV4, Transient receptor potential vanilloid 4; UCs, Urothelial cells

                Article
                DOI: 10.14440/bladder.2023.870
                PMC ID: 10668602
                SO-VID: 6d477691-2c29-4c7b-bdd1-ff84204e9c3c
                Copyright © © 2013-2023 Bladder, All rights reserved.
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License: http://creativecommons.org/licenses/by-nc-sa/4.0

                History
                Date received : 19 July 2023
                Date revision received : 15 September 2023
                Date accepted : 09 October 2023
                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 65, Pages: 12
                Categories
                Subject: Review

                Keywords: bladder dysfunction,mechanosensitive cation channels,piezo channels
                Data availability:
                Keywords: bladder dysfunction, mechanosensitive cation channels, piezo channels

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