Talk:Seminal Vesicle Development

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Cite this page: Hill, M.A. (2019, October 18) Embryology Seminal Vesicle Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Seminal_Vesicle_Development

2016

Seminal vesicle proteins SVS3 and SVS4 facilitate SVS2 effect on sperm capacitation

Reproduction. 2016 Oct;152(4):313-21. doi: 10.1530/REP-15-0551. Epub 2016 Aug 2.

Araki N1, Kawano N2, Kang W2, Miyado K3, Yoshida K4, Yoshida M5.

Abstract

Mammalian spermatozoa acquire their fertilizing ability in the female reproductive tract (sperm capacitation). On the other hand, seminal vesicle secretion, which is a major component of seminal plasma, inhibits the initiation of sperm capacitation (capacitation inhibition) and reduces the fertility of the capacitated spermatozoa (decapacitation). There are seven major proteins involved in murine seminal vesicle secretion (SVS1-7), and we have previously shown that SVS2 acts as both a capacitation inhibitor and a decapacitation factor, and is indispensable for in vivo fertilization. However, the effects of SVSs other than SVS2 on the sperm have not been elucidated. Since mouse Svs2-Svs6 genes evolved by gene duplication belong to the same gene family, it is possible that SVSs other than SVS2 also have some effects on sperm capacitation. In this study, we examined the effects of SVS3 and SVS4 on sperm capacitation. Our results showed that both SVS3 and SVS4 are able to bind to spermatozoa, but SVS3 alone showed no effects on sperm capacitation. On the other hand, SVS4 acted as a capacitation inhibitor, although it did not show decapacitation abilities. Interestingly, SVS3 showed an affinity for SVS2 and it facilitated the effects of SVS2. Interaction of SVS2 and spermatozoa is mediated by the ganglioside GM1 in the sperm membrane; however, both SVS3 and SVS4 had weaker affinities for GM1 than SVS2. Therefore, we suggest that separate processes may cause capacitation inhibition and decapacitation, and SVS3 and SVS4 act on sperm capacitation cooperatively with SVS2. © 2016 Society for Reproduction and Fertility. PMID 27486266

2013

Advantages of magnetic resonance imaging (MRI) of the seminal vesicles and intra-abdominal vas deferens in patients with congenital absence of the vas deferens

Urology. 2013 Aug;82(2):345-51. doi: 10.1016/j.urology.2013.03.038. Epub 2013 Jun 13.

Chiang HS1, Lin YH, Wu YN, Wu CC, Liu MC, Lin CM.

Abstract

OBJECTIVE: To show the flexibility in magnetic resonance imaging (MRI) of seminal vesicle (SV) and intra-abdominal segment of vas deferens for the patients with congenital absence of the vas deferens (CAVD), including congenital bilateral absence of the vas deferens (CBAVD) and congenital unilateral absence of vas deferens (CUAVD). METHODS: Fourteen consecutive patients with CAVD had transrectal ultrasonography (TRUS) and further MRI evaluations. TRUS was performed using a 7.5-MHz transducer, and images of the SVs were obtained, calculated in the transaxial plane. MRI studies were performed with a 1.5-7 superconducting system, T1- and T2-weighted axial, coronal, and sagittal imaging of the pelvis was obtained. If the SVs were present, then their size was measured for the morphologic classification and diagnosis. All of the patients also received cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation testing. RESULTS: In a series of 12 men with CBAVD, only 4 were found to have bilateral SV agenesis using MRI. The remaining 8 men with unilateral hypoplasia still had SV remnants. MRI also detected the intra-abdominal segment of the vas deferens. Through our study of MRI, SV agenesis is not well associated with the presence of CFTR mutation in patients with CAVD. CONCLUSION: MRI provides a precise imaginal diagnosis of SV defect, which is superior to the TRUS examination for the patients with CAVD. Compared with the previous inaccurate examination method of TRUS, this study demonstrates that MRI can provide better images for the patients with CAVD for the clinical diagnosis of existing defects of internal seminal tract and internal organs. Copyright © 2013 Elsevier Inc. All rights reserved.

PMID 23768522

Cysts of the lower male genitourinary tract: embryologic and anatomic considerations and differential diagnosis

Radiographics. 2013 Jul-Aug;33(4):1125-43. doi: 10.1148/rg.334125129.

Shebel HM1, Farg HM, Kolokythas O, El-Diasty T.

Abstract

Cysts of the lower male genitourinary tract are uncommon and usually benign. These cysts have different anatomic origins and may be associated with a variety of genitourinary abnormalities and symptoms. Various complications may be associated with these cysts, such as urinary tract infection, pain, postvoiding incontinence, recurrent epididymitis, prostatitis, and hematospermia, and they may cause infertility. Understanding the embryologic development and normal anatomy of the lower male genitourinary tract can be helpful in evaluating these cysts and in tailoring an approach for developing a differential diagnosis. There are two main groups of cysts of the lower male genitourinary tract: intraprostatic cysts and extraprostatic cysts. Intraprostatic cysts can be further classified into median cysts (prostatic utricle cysts, müllerian duct cysts), paramedian cysts (ejaculatory duct cysts), and lateral cysts (prostatic retention cysts, cystic degeneration of benign prostatic hypertrophy, cysts associated with tumors, prostatic abscess). Extraprostatic cysts include cysts of the seminal vesicle, vas deferens, and Cowper duct. A variety of pathologic conditions can mimic these types of cysts, including ureterocele, defect resulting from transurethral resection of the prostate gland, bladder diverticulum, and hydroureter and ectopic insertion of ureter. Accurate diagnosis depends mainly on the anatomic location of the cyst. Magnetic resonance imaging and transrectal ultrasonography (US) are excellent for detecting and characterizing the nature and exact anatomic origin of these cysts. In addition, transrectal US can play an important therapeutic role in the management of cyst drainage and aspiration, as in cases of prostatic abscess. © RSNA, 2013.

PMID 23842975

2014

Seminal vesicle hypoplasia with contralateral renal agenesis

Urology. 2014 Sep;84(3):e7. doi: 10.1016/j.urology.2014.05.013. Epub 2014 Jul 19.

Resorlu M1, Adam G2, Uysal F2, Bas S2, Karatag O2, Sancak EB3. Author information Abstract Renal agenesis is a rare condition of unknown etiology frequently seen together with ipsilateral seminal vesicle and vas deferens anomalies because of common embryologic development. However, no cases of contralateral seminal vesicle hypoplasia accompanying renal agenesis have previously been reported. We describe a case of contralateral seminal vesicle hypoplasia accompanying renal agenesis incidentally detected in a 27-year-old presenting to the urology clinic with pelvic pain.

Copyright © 2014 Elsevier Inc. All rights reserved.

PMID 25053522

2006

Branching morphogenesis in the prostate gland and seminal vesicles

Differentiation. 2006 Sep;74(7):382-92.

Thomson AA, Marker PC. Source MRC Human Reproductive Sciences Unit, 37 Chalmers Street, Edinburgh EH3 9ET, UK.

Abstract

The prostate gland and seminal vesicles are the major exocrine glands in the male reproductive tracts of mammals. Although the morphology of these organs varies widely among species, epithelial branching morphogenesis is a key feature of organ development in most mammals including rodents and humans. Insight into the mechanisms that control prostatic and seminal vesicle branching morphogenesis has come from experimental embryological work as well as from the study of mice and humans harboring mutations that alter branching morphogenesis. These studies have demonstrated a requirement for androgens to initiate branching morphogenesis as well as a role for androgens in sustaining the normal rate and extent of branching. In addition, these studies have revealed a series of reciprocal paracrine signals between the developing prostatic epithelium and prostatic mesenchyme that are essential for regulating branching morphogenesis. Key growth factors that participate in these signaling events include members of the fibroblast growth factor, Hedgehog, and transforming growth factor-beta families. Additional genes including several homeobox-containing transcription factors have also been implicated as key regulators of prostatic and seminal vesicle branching morphogenesis. While research in recent years has greatly enhanced our understanding of the molecular control of prostatic and seminal vesicle development, known genes cannot yet explain in molecular terms the complex biological interactions that descriptive and experimental embryological studies have elucidated in the control of branching morphogenesis in these organs.

PMID 16916376


2001

Dev Biol. 2001 Jun 1;234(1):138-50.

The BMP family member Gdf7 is required for seminal vesicle growth, branching morphogenesis, and cytodifferentiation

Settle S, Marker P, Gurley K, Sinha A, Thacker A, Wang Y, Higgins K, Cunha G, Kingsley DM. Source Department of Developmental Biology and Howard Hughes Medical Institute, Beckman Center B300, Stanford University School of Medicine, Stanford, California 94305-5427, USA.

Abstract

Epithelial-mesenchymal interactions play an important role in the development of many different organs and tissues. The secretory glands of the male reproductive system, including the prostate and seminal vesicles, are derived from epithelial precursors. Signals from the underlying mesenchyme are required for normal growth, branching, and differentiation of the seminal vesicle epithelium. Here, we show that a member of the BMP family, Gdf7, is required for normal seminal vesicle development. Expression and tissue recombination experiments suggest that Gdf7 is a mesenchymal signal that acts in a paracrine fashion to control the differentiation of the seminal vesicle epithelium. Copyright 2001 Academic Press.

PMID 11356025


Blue Histology - Seminal Vesicles

The seminal vesicles develop from the vas deferens. Their histological organisation resembles to some extent that of the vas deferens. They are elongated sacs (about 4 cm long and 2 cm wide), which taper where they unite with the vas deferens. Each seminal vesicle consists of one coiling tube (about 15cm long). All the lumina visible in sections of the seminal vesicle are in continuity in the intact organ.

The mucosa shows thin, branched, anastomosing folds. The structure of the epithelium is variable appearing columnar or pseudostratified columnar (columnar cells and basal cells). The lamina propria of the mucosa is fairly thin and loose. The muscularis consists of inner circular and outer longitudinal layers of smooth muscle.

Seminal vesicles were thought to store semen - hence there name. This turned out to be wrong. They are glands, whose secretion constitutes 60-70 % of the ejaculate. The secretory product of the columnar cell, which may be seen in the lumen of the seminal vesicles, is strongly acidophilic. It contains large amounts of fructose which the spermatozoa utilise as a source of energy. Furthermore, the secretion contains prostaglandins, flavins (yellow fluorescing pigment - of use in forensic medicine to detect semen stains) and several other proteins and enzymes.

The cocktail of compounds which is released by the seminal vesicles in addition to fructose has three main functions:

the formation of the sperm coagulum, the regulation of sperm motility and the suppression of immune function in the female genital tract. The secretion of the seminal vesicles is the third fraction of the ejaculate (the spermatozoa are released with the second fraction - the contents of the vas deferens).