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In mammals, sperm migrate through the female reproductive tract to reach the egg; however, our understanding of this journey is highly limited. To shed light on this process, we focused on defining the functions of seminal vesicle secretion 2 (SVS2). SVS2-/- male mice produced sperm but were severely subfertile, and formation of a copulatory plug to cover the female genital opening did not occur. Surprisingly, even when artificial insemination was performed with silicon as a substitute for the plug, sperm fertility in the absence of SVS2 remained severely reduced because the sperm were already dead in the uterus. Thus, our results provide evidence that the uterus induces sperm cell death and that SVS2 protects sperm from uterine attack.

Semenogelin 1 (SEMG1), a main component of human seminal plasma, is a multi-functional protein involved in the regulation of sperm motility and fertility. SEMG1 is orthologous to mouse seminal vesicle secretion 2 (SVS2), required for sperm survival in the female reproductive tract after copulation; however, its in vivo function remains unclear. In this study, we addressed this issue by examining the effect of recombinant SEMG1 on intrauterine mouse sperm survival. SEMG1 caused a dose-dependent decrease in mouse sperm motility, similar to its effect on human sperm, but SVS2 had no effect on mouse sperm motility. Mouse epididymal sperm in the presence of 100 µM SEMG1, a concentration that does not affect mouse sperm motility, were injected into the mouse uterus (intrauterine insemination, IUI). IUI combined with SEMG1 significantly increased the survival rate of intrauterine mouse sperm. The effect of SEMG1 on intrauterine sperm survival was comparable with that of SVS2. For clinical applications, three potentially sperm-protecting polypeptides that are easy to handle were designed from SEMG1, but their individual use was unable to mimic the ability of SEMG1. Our results indicate that SEMG1 has potential clinical applications for effective IUI and thereby for safe, simple, and effective internal fertilization.

Multiple genes, whose functions or expression are overlapping, compensate for the loss of one gene. A gene cluster in the mouse genome encodes five seminal vesicle proteins (SVS2, SVS3, SVS4, SVS5, and SVS6). These proteins are produced by male rodents and function in formation of the copulatory plug following mating. SVS2 plays an essential role in the successful internal fertilization by protecting the sperm membrane against a uterine immune attack. We hypothesized that the four remaining seminal vesicle proteins (SVPs) of this gene cluster may partially/completely compensate for the deficiency of SVS2. For confirming our hypothesis, we generated mice lacking the entire SVP-encoding gene cluster and compared their fecundity with Svs2-deficient (Svs2−/−) mice; that is, mice deficient in Svs2 alone. A single loxP site remained after the deletion of the Svs2 gene. Therefore, we inserted another loxP site by combining the CRISPR/Cas9 system with single-stranded oligodeoxynucleotides (ssODN). Male mice lacking the entire SVP-encoding gene cluster (Svs2–6−/− mice) and thereby all five SVP proteins, generated by the deletion of 100kbp genomic DNA, showed low fecundity. However, the fecundity level was comparable with that from Svs2−/− male mice. Our results demonstrate that SVS3, SVS4, SVS5, and SVS6 do not function in the protection of sperm against a uterine immune attack in the absence of SVS2. Thus, Svs2 is the critical gene in the SVP gene cluster.

PurposeProstate-specific antigen (PSA) is thought to be undetectable (< 0.1 ng/mL) after radical prostatectomy (RP), and persistent PSA (≥ 0.1 ng/mL) is considered a failure of curative treatment.Materials and MethodsThe study population consisted of 135 patients, all of whom underwent RP for localized prostate cancer, and developed persistent PSA. We set the starting point at the timing of RP, and the endpoints were the development of castration-resistant prostate cancer (CRPC) and cancer-specific survival.ResultsSalvage radiation therapy (RT) and androgen deprivation therapy (ADT) were performed in 53 (39.3%) and 64 (47.4%) patients, respectively. Eighteen (13.3%) patients didn't receive any salvage treatment. During the median follow-up of 10.1 years, CRPC was observed in 23 patients, and 6 patients died due to prostate cancer. Kaplan-Meier curves demonstrated the 15-year CRPC-free and cancer-specific survivals were 79.5% and 92.7%, respectively. Cox multivariate analysis demonstrated that seminal vesicle invasion (SVI) (p = 0.007) and nadir PSA ≥1.0 ng/mL (p = 0.002) were independent risk factors for CRPC. Salvage RT demonstrated better cancer control (the 10-and 15-year CRPC-free survival was 94.1% and 94.1%) compared to ADT (75.9% and 58.5%, p = 0.017) after 1:1 propensity score matching.ConclusionsSVI and nadir PSA ≥1.0 ng/mL are independent risk factors for CRPC in patients with persistent PSA after RP. Salvage RT is considered to be the optimal treatment for this condition.

Zinner syndrome is a rare congenital urological entity, secondary to an alteration in embryogenesis between 4th and 13th weeks of gestation, specifically because of abnormalities in the development of the distal mesonephric duct. It is characterized by the triad of unilateral renal agenesis, cystic dilatation of the ipsilateral seminal vesicle and ipsilateral ejaculatory duct obstruction. The aim of this article is to provide the reader with all the necessary information to be able to suspect the presence of this syndrome, reviewing its physiopathology, clinical manifestations and the imaging techniques that enable its diagnosis, emphasizing those radiological findings by MRI that should lead us to think about it. This work is illustrated with representative radiological images of cases belonging to our institution, including patients with different variants of Zinner syndrome. We also include an overview of the embryology of the male urogenital system, to remember the role of the mesonephric duct and the ureteral bud in the formation of the different urogenital structures, as well as a differential diagnosis that allows us to differentiate seminal vesicle cysts from other pelvic cystic lesions.

Seminal plasma (SP) is rich in extracellular vesicles (EVs), which are still poorly studied, especially in livestock species. To better understand their functional role in both spermatozoa and endometrial epithelial cells, proper characterization of EVs is an essential step. The objective was to phenotypically characterize porcine seminal EVs (sEVs) using cryogenic electron microscopy (cryo-EM), which allows visualization of EVs in their native state. Porcine ejaculates are released in fractions, each containing SP from different source. This allows characterization sEVs released from various male reproductive tissues. Two experiments were performed, the first with SP from the entire ejaculate (n:6) and the second with SP from three ejaculate fractions (n:15): the first 10 mL of the sperm-rich ejaculate fraction (SRF-P1) with SP mainly from the epididymis, the remainder of the SRF (SRF-P2) with SP mainly from the prostate, and the post-SRF with SP mainly from the seminal vesicles. The sEVs were isolated by size exclusion chromatography and 1840 cryo-EM sEV images were acquired using a Jeol-JEM-2200FS/CR-EM. The size, electron density, complexity, and peripheral corona layer were measured in each sEV using the ImageJ software. The first experiment showed that sEVs were structurally and morphologically heterogeneous, although most (83.1%) were small (less than 200 nm), rounded, and poorly electrodense, and some have a peripheral coronal layer. There were also larger sEVs (16.9%) that were irregularly shaped, more electrodense, and few with a peripheral coronal layer. The second experiment showed that small sEVs were more common in SRF-P1 and SRF-P2, indicating that they originated mainly from the epididymis and prostate. Large sEVs were more abundant in post-SRF, indicating that they originated mainly from seminal vesicles. Porcine sEVs are structurally and morphologically heterogeneous. This would be explained by the diversity of reproductive organs of origin.

Diabetes is a detriment to male reproductive health, notably through its capacity to diminish secretion from accessory glands such as the seminal vesicles and prostate, which are crucial for reproductive function. Curcumin, a naturally derived polyphenol renowned for its anti-inflammatory and antioxidative attributes, has demonstrated potential in mitigating tissue damage across various organs in diabetic patients. Despite its established benefits, the specific impact of curcumin on seminal vesicle damage in the context of diabetes remains underexplored. This investigation delves into the therapeutic potential of curcumin in ameliorating seminal vesicle damage in diabetic rats, thereby elucidating its underlying mechanisms. This study focused on twenty male SD rats divided into two distinct groups, a control cohort and a diabetic contingent, and employed a streptozocin (STZ)-induced type 1 diabetic rat model to ascertain seminal vesicle alterations secondary to diabetes. Ultrasonography was used to measure rat seminal vesicle sizes for comparison with postdissection measurements. This study revealed that (1) seminal vesicle volume and seminal fluid secretion were reduced in diabetic rats and (2) ultrasonography can predict seminal vesicle secretory dysfunction in diabetic rats, providing a theoretical basis for selecting animal models of diabetic seminal vesicle dysfunction for subsequent studies. Thirty male SD rats were subsequently divided into three groups: control, diabetic, and curcumin-treated. The curcumin group, which was subjected to a one-month-long intervention after STZ-induced diabetes onset, exhibited significant histological and functional recovery. Haematoxylin‒eosin (HE) staining revealed disordered seminal vesicle tissue structures and decreased epithelial cell height in diabetic rats, which was partially restored after curcumin treatment. Western blot and PCR results demonstrated that the expression levels of androgen receptor (AR) and aquaporin (AQP)8 in the seminal vesicle tissues of diabetic rats were decreased, whereas curcumin treatment led to increases in the expression levels of AR and AQP8. Seminal vesicle cells were cultured in vitro and divided into six groups: control, HG, HG-CUR-5 µM, HG-CUR-10 µM, HG-CUR-20 µM, and HG-CUR-50 µM. After 48 h of intervention, the fructose concentration in the culture medium was measured, and the expression of AR and AQP8 in the control, HG, and HG-CUR-20 µM groups was determined via Western blotting and PCR. The results revealed that the expression of AR and APQ8 in high glucose-treated seminal vesicle cells was decreased and that curcumin treatment upregulated the expression of AR and AQP8. After the addition of bicalutamide (an AR inhibitor), the expression of AQP8 was reduced. These findings suggest that curcumin may alleviate seminal vesicle damage in type 1 diabetic rats by activating the AR-AQP8 pathway.

Background Mixed epithelial and stromal tumors (MESTs) of the seminal vesicle are exceptionally rare neoplasms composed of both epithelial and stromal elements, posing significant diagnostic challenges due to their rarity and overlapping characteristics with other pelvic neoplasms. Case presentation We describe a 45-year-old patient with chronic pelvic pain and obstructive urinary symptoms. Imaging revealed a large cystic and solid mass involving his seminal vesicles, with significant mass effect on adjacent structures. Differential diagnoses included seminal vesicle adenocarcinoma and sarcoma. Complete surgical resection and subsequent histopathological analysis confirmed a low-grade seminal vesicle MEST with biphasic epithelial and stromal components, lacking atypia or notable mitotic activity. Immunohistochemical analysis revealed stromal positivity for estrogen receptor (ER), progesterone receptor (PR), smooth muscle actin, desmin, and CD34, and epithelial positivity for PAX8, PAX2, CK7, and MUC-6, supporting the diagnosis. The patient remains disease-free 32 months post-surgery. Conclusion Seminal vesicle MESTs are rare and histologically diverse tumors, with pathogenesis likely hormonally influenced given ER and PR expression. Diagnosis requires a multidisciplinary approach, including imaging, histopathology, and immunohistochemistry. Surgical excision is the preferred treatment, offering an excellent prognosis for low-grade cases. This case emphasizes the importance of detailed documentation to improve understanding and management of these rare tumors, and its prognosis.

Background Solitary fibrous tumors (SFTs) are rare mesenchymal tumors that can occur in multiple parts of the human body. The majority of SFTs are benign, with malignant cases being exceedingly rare. Although SFTs have been identified in extrapleural sites such as the upper respiratory tract, orbits, and extremities, their occurrence in the seminal vesicles is exceedingly uncommon. To date, only a few cases of seminal vesicle SFTs have been documented, making this case notable for its rarity and clinical presentation. Case presentation A 43-year-old male patient was incidentally found to have a left seminal vesicle mass on an MRI scan during a routine health check-up. A subsequent PET‒CT scan revealed enlargement of the left seminal vesicle with uneven density and FDG uptake, raising suspicion of malignancy. Although a biopsy suggested a solitary fibrous tumor of the seminal vesicle, the limited tissue sample prevented definitive exclusion of malignancy. This highlights the diagnostic challenges of such rare tumors, particularly when biopsy samples are insufficient. To address this, rapid intraoperative pathology was employed, which confirmed the malignancy and informed the patient of the subsequent surgical approach. The patient underwent laparoscopic excision of the left seminal vesicle tumor, followed by radical excision of both the prostate and seminal vesicles. Postoperatively, the patient recovered well, and final pathology confirmed a malignant solitary fibrous tumor. After five years of follow-up, the patient remained free from recurrence or metastasis. Conclusion Although the preoperative biopsy in this case established the diagnosis of SFT, it did not definitively ascertain whether it was benign or malignant. Hence, intraoperative frozen section pathology plays a critical role in determining the surgical strategy. This case indicates that satisfactory therapeutic outcomes for seminal vesicle SFTs can be achieved through complete resection via minimally invasive laparoscopic surgery.

Background: Dexamethasone (DEX) has recently been used to treat inflammation and to induce the chronic stress (CS) in animal models. Although its adverse effects on testicular damage and seminal plasma reduction were previously reported, the changes in the seminal vesicle are still unexplored. This study aimed to investigate the effects of DEX on biochemical alterations in seminal vesicle fluid (SVF) and seminal vesicle tissue (SVT). Methods: Male rats were divided into control and DEX groups ( n = 20). CS animals were induced with DEX at 1.5 mg/KgBW for 21 consecutive days. CS behaviors were confirmed by the tests of tail suspension, forced swimming, and sucrose preference. Hormones and biochemical components in serum and SVF were evaluated. SVF volume and histomorphometry of SVT were observed. Expressions of apoptotic markers and seminal vesicle secreting protein 4 (SVS4) were determined. Results: The results showed the reductions of seminal vesicle size and SVF volume in DEX rats. DEX increased the malondialdehyde (MDA) level in SVF, and DNA fragmentation revealed by the TUNEL assay. Serum testosterone and levels of magnesium and fructosamine in SVF of the DEX group were significantly decreased. DEX altered the thickness of the seminal vesicle wall. The expression of SVS4 was decreased in SVT induced with DEX. However, no difference in apoptotic expressions (Hsp70, procaspase‐3, and procaspase‐9) was observed between groups. Conclusion: The DEX‐induced CS caused the seminal vesicle changes, which were associated with DNA fragmentation. Decreases of fructosamine and SVS4 may be a cause of low‐sperm quality such as motility and capacitation in CS men.