Penile apoptosis in association with p53 under lack of testosterone

Yamamoto, Hiroto; Sasaki, Shoichi; Tatsura, Hiroyuki; Umemoto, Yukihiro; Kubota, Hirokazu; Kamiya, Hiroyuki; Kawai, Tetsuya; Kang, Ki-Ho; Kohri, Kenjiro

doi:10.1007/s00240-003-0358-6

Cited by 14 publications

(11 citation statements)

References 18 publications

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“…This report suggested that low plasma testosterone levels were associated with EDys in men, independently of the presence of other VRFs, corroborating the idea that testosterone has a protective effect in endothelial functionality [32]. At penile level, studies in animal models suggested that testosterone deficiency is associated to apoptosis of cavernosal vascular ECs [48] and that testosterone replacement therapy was able to induce CC cell proliferation and endothelial DNA synthesis [49]. Additionally, testosterone has been suggested to modulate several pathways on different erectile tissue components crucial for normal erection.…”

Section: Testosterone Endothelial Health and Erectionmentioning

confidence: 52%

Testosterone, Endothelial Health, and Erectile Function

2011

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Experimental and clinical studies have reported that testosterone has a critical role in the maintenance of homeostatic and morphologic corpus cavernosum components, essential for normal erectile physiology. Although the exact mechanisms mediated by testosterone in erectile function are still under investigation, recent research has suggested an important role in the regulation of endothelial cell (EC) biological functions. Besides stimulating the production of EC mediators, testosterone is also thought to promote the vasculogenic reendothelialization process, mediated by bone marrow-derived endothelial progenitor cells. Additionally, testosterone seems to modulate other erectile tissue components, including trabecular smooth muscle cells, nerve fibers, and tunica albuginea structure, all essential for the erectile process. This paper summarizes current data regarding testosterone-induced cellular and molecular mechanisms that regulate penile tissue components, focusing particularly on the role of testosterone in endothelial health and erectile function.

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Section: Testosterone Endothelial Health and Erectionmentioning

confidence: 52%

Testosterone, Endothelial Health, and Erectile Function

2011

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“…For experiment 1, the animals were injected subcutaneously with either 0.9% saline (vehicle; Sigma-Aldrich, St. Louis, MO) or LEU (1.2mg/kg; Sigma-Aldrich, St. Louis, MO) thirty minutes before the extinction session on day 2. The 1.2mg/kg dose was selected based on results from our dose response test to confirm this was the lowest dose to induce the T surge, as well as previous reports examining the castration effects of LEU with chronic administration at doses from 1–3mg/kg for days to months (Ichikawa et al, 1988; Kostanski et al, 2000; Yamamoto et al, 2004). On day 3 for both experiments, the animals were returned to the chamber and presented with 3 CS-alone trials for the extinction recall test.…”

Section: Methodsmentioning

confidence: 99%

Acute gonadotropin-releasing hormone agonist treatment enhances extinction memory in male rats

Maeng

Taha

Cover

et al. 2017

Psychoneuroendocrinology

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Leuprolide acetate (LEU), also known as Lupron, is commonly used to treat prostate cancer in men. As a gonadotropin-releasing hormone (GnRH) receptor agonist, it initially stimulates the release of gonadal hormones, testosterone (T) and estradiol. This surge eventually suppresses these hormones, preventing the further growth and spread of cancer cells. Individuals receiving this treatment often report anxiety and cognitive changes, but LEU’s effects on the neural mechanisms that are involved in anxiety during the trajectory of treatment are not well known. In this study, we examined the acute effects of LEU on fear extinction, hypothesizing that increased T levels following a single administration of LEU will facilitate extinction recall by altering neuronal activity within the fear extinction circuitry. Two groups of naïve adult male rats underwent a 3-day fear conditioning, extinction, and recall experiment. The delayed group (n=15) received a single injection of vehicle or LEU (1.2mg/kg) 3 weeks before behavioral testing. The acute group (n=25) received an injection one day after fear conditioning, 30 minutes prior to extinction training. Following recall, the brains for all animals were collected for c-fos immunohistochemistry. Blood samples were also collected and assayed for T levels. Acute administration of LEU increased serum T levels during extinction training and enhanced extinction recall 24h later. This enhanced extinction memory was correlated with increased c-fos activity within the infralimbic cortex and amygdala, which was not observed in the delayed group. These results suggest that the elevation in T induced by acute administration of LEU can influence extinction memory consolidation, perhaps through modification of neuronal activity within the infralimbic cortex and amygdala. This may be an important consideration in clinical applications of LEU and its effects on anxiety and cognition.

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“…A remodeling process occurs in the penis of castrated rats that involves apoptosis of the erectile tissue [20–23]. Zhang et al.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Testosterone Effects on Sonic Hedgehog Signaling in Juvenile, Adolescent and Adult Sprague Dawley Rat Penis

Bond

Angeloni

Podlasek

2010

The Journal of Sexual Medicine

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Introduction Smooth muscle apoptosis is a major contributing factor to erectile dysfunction (ED) development in prostatectomy and diabetic patients and animal models. A critical regulator of penile smooth muscle and apoptosis is Sonic hedgehog (SHH). The SHH protein is decreased in ED models and SHH treatment of cavernous nerve (CN) injured rats prevents smooth muscle apoptosis. A close association between androgen deficiency and ED has been suggested in the literature, but few studies have examined the molecular effects on penile smooth muscle and on known signaling mechanisms that regulate morphology. Aim Examine testosterone and SHH interaction in eugonadal adult, adolescent and juvenile rats by performing castration studies and treatment with supraphysiological testosterone. Methods The eugonadal adult Sprague Dawley rats were either treated with testosterone for 7 or 14 days (N=14) or were castrated for 4 or 7 days (N=12). The juvenile rats were treated with testosterone for 8 days (N=7). The adolescent rats were castrated and sacrificed at P88 (N=8). The control rats had empty vehicle (N=22) or sham surgery (N=20). Main Outcome Measures The active form of SHH protein and mRNA were quantified by semi-quantitative immunohistochemical analysis and real-time reverse transcriptase polymerase chain reaction (RT-PCR). Results Testosterone treatment did not alter SHH signaling in juvenile rats. Shh mRNA increased 3.2-fold and SHH protein increased 1.2-fold in rats castrated during puberty. In adult rats, castration decreased Shh mRNA 3.2-fold but did not alter SHH protein. Testosterone supplement in adult rats increased Shh mRNA 2.3-fold and decreased SHH protein 1.3-fold. Conclusions SHH signaling is independent of testosterone in normal juvenile rats and is sensitive to testosterone during adolescence, while testosterone supplement in the adult adversely impacts SHH signaling in a very similar manner to that observed with CN injury.

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Penile apoptosis in association with p53 under lack of testosterone

Cited by 14 publications

References 18 publications

Testosterone, Endothelial Health, and Erectile Function

Testosterone, Endothelial Health, and Erectile Function

Acute gonadotropin-releasing hormone agonist treatment enhances extinction memory in male rats

Analysis of Testosterone Effects on Sonic Hedgehog Signaling in Juvenile, Adolescent and Adult Sprague Dawley Rat Penis

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