scholarly journals Somatostatin immunoreactivity within the urinary bladder nerve fibers and paracervical ganglion urinary bladder projecting neurons in the female pig

2021 ◽  
pp. 102007
Author(s):  
Urszula Mazur ◽  
Ewa Lepiarczyk ◽  
Paweł Janikiewicz ◽  
Agnieszka Bossowska
Keyword(s):  
Urinary Bladder ◽  
Nerve Fibers ◽  
Somatostatin Immunoreactivity

scholarly journals Dystrophin is expressed in smooth muscle and afferent nerve fibers in the rat urinary bladder

2019 ◽  
Vol 60 (2) ◽  
pp. 202-210 ◽  
Author(s):  
Judith M. Lionarons ◽  
Govert Hoogland ◽  
Ruben G. F. Hendriksen ◽  
Catharina G. Faber ◽  
Danique M. J. Hellebrekers ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Rat Urinary Bladder ◽  
Afferent Nerve Fibers

Phosphorylation of extracellular signal-regulated kinases in urinary bladder in rats with cyclophosphamide-induced cystitis

2007 ◽  
Vol 293 (1) ◽  
pp. R125-R134 ◽  
Author(s):  
Kimberly A. Corrow ◽  
Margaret A. Vizzard
Keyword(s):  
Urinary Bladder ◽  
Chronic Treatment ◽  
Bladder Capacity ◽  
Nerve Fibers ◽  
Bladder Function ◽  
Detrusor Smooth Muscle ◽  
Erk Phosphorylation ◽  
Extracellular Signal ◽  
Perk Expression ◽  
Whole Mount

Phosphorylated ERK expression has been demonstrated in the central and peripheral nervous system after various stimuli, including visceral stimulation. Changes in the activation (i.e., phosphorylation) of extracellular signal-regulated kinases (pERK) were examined in the urinary bladder after 4 h (acute), 48 h (intermediate), or chronic (10 day) cyclophosphamide (CYP) treatment. CYP-induced cystitis significantly ( P ≤ 0.01) increased pERK expression in the urinary bladder with intermediate (48 h) and chronic CYP treatment. Immunohistochemistry for pERK immunoreactivity revealed little pERK-IR in control or acute (4 h) CYP-treated rat urinary bladders. However, pERK expression was significantly ( P ≤ 0.01) upregulated in the urothelium after 48 h or chronic CYP treatment. Whole mount preparations of urothelium/lamina propria or detrusor smooth muscle from control (noninflamed) rats showed no pERK-IR in PGP9.5-labeled nerve fibers in the suburothelial plexus. However, with CYP-treatment (48 h, chronic), a few pERK-IR nerve fibers in the suburothelial plexus of whole mount preparations of bladder and at the serosal edge of urinary bladder sections were observed. pERK-IR cells expressing the CD86 antigen were also observed in urinary bladder from CYP-treated rats (48 h, chronic). Treatment with the upstream inhibitor of ERK phosphorylation, U0126, significantly ( P ≤ 0.01) increased bladder capacity in CYP-treated rats (48 h). These studies suggest that therapies targeted at pERK pathways may improve urinary bladder function in CYP-treated rats.

scholarly journals Expression of cyclooxygenase-2 in urinary bladder in rats with cyclophosphamide-induced cystitis

2007 ◽  
Vol 293 (2) ◽  
pp. R677-R685 ◽  
Author(s):  
Mary Beth Klinger ◽  
Abbey Dattilio ◽  
Margaret A. Vizzard
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Inflammatory Cell ◽  
Nerve Fibers ◽  
Cyclooxygenase 2 ◽  
Detrusor Smooth Muscle ◽  
Cox 2

These studies examined the expression of cyclooxygenase-2 (COX-2) expression in the urothelium and suburothelial space and detrusor from rats treated with cyclophosphamide (CYP) to induce acute (4 h), intermediate (48 h), or chronic (10-day) cystitis. Western blot analysis and immunohistochemistry were used to demonstrate COX-2 expression. In whole mount preparations of urinary bladder, nerve fibers in the suburothelial plexus, and inflammatory cell infiltrates were characterized for COX-2 expression after CYP-induced cystitis. COX-2 expression significantly ( P ≤ 0.01) increased in the urothelium + suburothelium and detrusor smooth muscle with acute, intermediate, and chronic (10-day) CYP-induced cystitis, but expression in urothelium + suburothelium was significantly greater. CYP-induced upregulation of COX-2 showed by immunostaining in the urothelium + suburothelium was similar to that observed with Western blot analysis and also demonstrated COX-2 inflammatory cell infiltrates (CD86+) and nerve fibers (PGP+) in the suburothelial plexus. Although COX-2 expression was significantly ( P ≤ 0.01) increased in detrusor smooth muscle, immunohistochemistry failed to demonstrate an obvious change in COX-2-immunoreactivity (IR) in detrusor muscle, but COX-2 inflammatory infiltrates were present throughout the detrusor. COX-2-IR nerve fibers exhibited increased density in the suburothelial plexus with acute or chronic CYP-induced cystitis. COX-2-IR macrophages (CD86+) were present throughout the urinary bladder with acute and chronic CYP-induced cystitis. These studies demonstrate cellular targets in the urinary bladder where COX-2 inhibitors may act.

scholarly journals Overexpression of NGF in mouse urothelium leads to neuronal hyperinnervation, pelvic sensitivity, and changes in urinary bladder function

2010 ◽  
Vol 298 (3) ◽  
pp. R534-R547 ◽  
Author(s):  
Birthe Schnegelsberg ◽  
Tung-Tien Sun ◽  
Gary Cain ◽  
Anindya Bhattacharya ◽  
Philip A. Nunn ◽  
...  
Keyword(s):  
Mast Cells ◽  
Urinary Bladder ◽  
Transgenic Mice ◽  
Bladder Dysfunction ◽  
Sympathetic Neurons ◽  
Nerve Fibers ◽  
Bladder Function ◽  
Sensory Afferents ◽  
Urinary Bladder Dysfunction

NGF has been suggested to play a role in urinary bladder dysfunction by mediating inflammation, as well as morphological and functional changes, in sensory and sympathetic neurons innervating the urinary bladder. To further explore the role of NGF in bladder sensory function, we generated a transgenic mouse model of chronic NGF overexpression in the bladder using the urothelium-specific uroplakin II (UPII) promoter. NGF mRNA and protein were expressed at higher levels in the bladders of NGF-overexpressing (NGF-OE) transgenic mice compared with wild-type littermate controls from postnatal day 7 through 12–16 wk of age. Overexpression of NGF led to urinary bladder enlargement characterized by marked nerve fiber hyperplasia in the submucosa and detrusor smooth muscle and elevated numbers of tissue mast cells. There was a marked increase in the density of CGRP- and substance P-positive C-fiber sensory afferents, neurofilament 200-positive myelinated sensory afferents, and tyrosine hydroxylase-positive sympathetic nerve fibers in the suburothelial nerve plexus. CGRP-positive ganglia were also present in the urinary bladders of transgenic mice. Transgenic mice had reduced urinary bladder capacity and an increase in the number and amplitude of nonvoiding bladder contractions under baseline conditions in conscious open-voiding cystometry. These changes in urinary bladder function were further associated with an increased referred somatic pelvic hypersensitivity. Thus, chronic urothelial NGF overexpression in transgenic mice leads to neuronal proliferation, focal increases in urinary bladder mast cells, increased urinary bladder reflex activity, and pelvic hypersensitivity. NGF-overexpressing mice may, therefore, provide a useful transgenic model for exploring the role of NGF in urinary bladder dysfunction.

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