Therapeutic effects of nerve growth factor‐targeting therapy on bladder overactivity in rats with prostatic inflammation

Igarashi, Taro; Tyagi, Pradeep; Mizoguchi, Shinsuke; Saito, Tetsuichi; Furuta, Akira; Suzuki, Yoshito; Egawa, Shin; Wang, Zhou; Yoshimura, Naoki

doi:10.1002/pros.24227

Cited by 10 publications

(16 citation statements)

References 23 publications

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“…It was found that chronic prostatitis excited its afferent nerves and increased transient receptor potential vanilloid1 (TRPV1) channel expression in L6-S1 DRG. It results in afferent neurons hyperexcitability, NGF up-regulation of bladders and prostates, and bladder abnormality [ 60 ]. Furthermore, it was observed in CP/CPPS that NGF was up-regulated, and the parasympathetic function of bladders was activated and sensitized following DRG excitement [ 41 ].…”

Section: Autonomic Nervous System Dysfunction’s Close Relation With C...mentioning

confidence: 99%

Autonomic Nervous System Dysfunction Is Related to Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Luo

Qian

et al. 2024

World J Mens Health

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Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common and non-lethal urological condition with painful symptoms. The complexity of CP/CPPS’s pathogenesis and lack of efficient etiological diagnosis results in incomplete treatment and recurrent episodes, causing long-term mental and psychological suffering in patients. Recent findings indicate that the autonomic nervous system involves in CP/CPPS, including sensory, sympathetic, parasympathetic, and central nervous systems. Neuro-inflammation and sensitization of sensory nerves lead to persistent inflammation and pain. Sympathetic and parasympathetic alterations affect the cardiovascular and reproductive systems and the development of prostatitis. Central sensitization lowers pain thresholds and increases pelvic pain perception in chronic prostatitis. Therefore, this review summarized the detailed processes and mechanisms of the critical role of the autonomic nervous system in developing CP/CPPS. Furthermore, it describes the neurologically relevant substances and channels or receptors involved in this process, which provides new perspectives for new therapeutic approaches to CP/CPPS.

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Section: Autonomic Nervous System Dysfunction’s Close Relation With C...mentioning

confidence: 99%

Autonomic Nervous System Dysfunction Is Related to Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Luo

Qian

et al. 2024

World J Mens Health

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“…Finally, it has been reported that prostatic inflammation is an important factor of LUTS in patients with BPH and that the degree of prostatic inflammation in BPH specimens is associated with the severity of LUTS [ 154 , 155 ]. Accordingly, animal models of prostatic inflammation induced by chemical irritation in rats or prostatic epithelium-specific deletion of E-cadherin in mice showed that prostatic inflammation-induced bladder overactivity due to prostate-to-bladder pelvic organ cross-sensitization through afferent hyperexcitability, which is mediated at least in part by NGF upregulation in the bladder [ 156 - 159 ]. Thus, local inflammation in the prostate seems to be an important factor inducing male LUTS in BPH patients.…”

Section: Pathological Conditions Underlying Oabmentioning

confidence: 99%

Pathophysiology of Overactive Bladder and Pharmacologic Treatments Including β3-Adrenoceptor Agonists -Basic Research Perspectives-

Kwon,

Kim,

Cho

et al. 2024

Int Neurourol J

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Overactive bladder (OAB) is a symptom-based syndrome defined by urinary urgency, frequency, and nocturia with or without urge incontinence. The causative pathology is diverse; including bladder outlet obstruction (BOO), bladder ischemia, aging, metabolic syndrome, psychological stress, affective disorder, urinary microbiome, localized and systemic inflammatory responses, etc. Several hypotheses have been suggested as mechanisms of OAB generation; among them, neurogenic, myogenic, and urothelial mechanisms are well-known hypotheses. Also, a series of local signals called autonomous myogenic contraction, micromotion, or afferent noises, which can occur during bladder filling, may be induced by the leak of acetylcholine (ACh) or urothelial release of adenosine triphosphate (ATP). They can be transmitted to the central nervous system through afferent fibers to trigger coordinated urgency-related detrusor contractions. Antimuscarinics, commonly known to induce smooth muscle relaxation by competitive blockage of muscarinic receptors in the parasympathetic postganglionic nerve, have a minimal effect on detrusor contraction within therapeutic doses. In fact, they have a predominant role in preventing signals in the afferent nerve transmission process. β3-adrenergic receptor (AR) agonists inhibit afferent signals by predominant inhibition of mechanosensitive Aδ-fibers in the normal bladder. However, in pathologic conditions such as spinal cord injury, it seems to inhibit capsaicin-sensitive C-fibers. Particularly, mirabegron, a β3-agonist, prevents ACh release in the BOO-induced detrusor overactivity model by parasympathetic prejunctional mechanisms. A recent study also revealed that vibegron may have 2 mechanisms of action: inhibition of ACh from cholinergic efferent nerves in the detrusor and afferent inhibition via urothelial β3-AR.

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“…Igarashi et al reported that nerve growth factor, locally expressed in the bladder, is an important mediator inducing bladder overactivity with the upregulation of C-fiber afferent markers following 5% formalin-induced prostate inflammation in a rat model. Thus, the cross-sensitization between the prostate and the bladder causes the complexity of CP/CPPS symptoms [ 3 ]. Persistent pain not only leads to physical discomfort but also affects the psychological state and prevents people from working, thus placing a financial burden on patients and society [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Low-Energy Shock Wave Suppresses Prostatic Pain and Inflammation by Modulating Mitochondrial Dynamics Regulators on a Carrageenan-Induced Prostatitis Model in Rats

Wang

Lee

et al. 2023

IJMS

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A low-energy shock wave (LESW) has therapeutic effects on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS); however, its mechanism of action remains unclear. We explored the effects of LESW on the prostate and mitochondrial dynamics regulators in a rat model of carrageenan-induced prostatitis. The imbalance of mitochondrial dynamics regulators may affect the inflammatory process and molecules and contribute to CP/CPPS. Male Sprague–Dawley rats received intraprostatic 3% or 5% carrageenan injections. The 5% carrageenan group also received LESW treatment at 24 h, 7 days, and 8 days. Pain behavior was evaluated at baseline, 1 week, and 2 weeks after a saline or carrageenan injection. The bladder and the prostate were harvested for immunohistochemistry and quantitative reverse-transcription polymerase chain reaction analysis. Intraprostatic carrageenan injection induced inflammatory reaction in the prostate and the bladder, decreased the pain threshold, and resulted in the upregulation of Drp-1, MFN-2, NLRP3 (mitochondrial integrity markers), substance P, and CGRP-RCP, whose effects were maintained for 1–2 weeks. LESW treatment suppressed carrageenan-induced prostatic pain, inflammatory reaction, mitochondrial integrity markers, and expression of sensory molecules. These findings support a link between the anti-neuroinflammatory effects of LESW in CP/CPPS and the reversal of cellular perturbations caused by imbalances in mitochondrial dynamics in the prostate.

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Therapeutic effects of nerve growth factor‐targeting therapy on bladder overactivity in rats with prostatic inflammation

Cited by 10 publications

References 23 publications

Autonomic Nervous System Dysfunction Is Related to Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Autonomic Nervous System Dysfunction Is Related to Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Pathophysiology of Overactive Bladder and Pharmacologic Treatments Including β3-Adrenoceptor Agonists -Basic Research Perspectives-

Low-Energy Shock Wave Suppresses Prostatic Pain and Inflammation by Modulating Mitochondrial Dynamics Regulators on a Carrageenan-Induced Prostatitis Model in Rats

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