scholarly journals Transcriptomic analysis of the seminal vesicle response to the reproductive toxicant acrylamide

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
David A. Skerrett-Byrne ◽  
Brett Nixon ◽  
Elizabeth G. Bromfield ◽  
James Breen ◽  
Natalie A. Trigg ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Seminal Vesicle ◽  
Reproductive Tract ◽  
Seminal Vesicles ◽  
Female Reproductive Tract ◽  
Complement Factor ◽  
Transcriptomic Response ◽  
Expression Of Genes ◽  
Chemokine Ligand ◽  
Type V

Abstract Background The seminal vesicles synthesise bioactive factors that support gamete function, modulate the female reproductive tract to promote implantation, and influence developmental programming of offspring phenotype. Despite the significance of the seminal vesicles in reproduction, their biology remains poorly defined. Here, to advance understanding of seminal vesicle biology, we analyse the mouse seminal vesicle transcriptome under normal physiological conditions and in response to acute exposure to the reproductive toxicant acrylamide. Mice were administered acrylamide (25 mg/kg bw/day) or vehicle control daily for five consecutive days prior to collecting seminal vesicle tissue 72 h following the final injection. Results A total of 15,304 genes were identified in the seminal vesicles with those encoding secreted proteins amongst the most abundant. In addition to reproductive hormone pathways, functional annotation of the seminal vesicle transcriptome identified cell proliferation, protein synthesis, and cellular death and survival pathways as prominent biological processes. Administration of acrylamide elicited 70 differentially regulated (fold-change ≥1.5 or ≤ 0.67) genes, several of which were orthogonally validated using quantitative PCR. Pathways that initiate gene and protein synthesis to promote cellular survival were prominent amongst the dysregulated pathways. Inflammation was also a key transcriptomic response to acrylamide, with the cytokine, Colony stimulating factor 2 (Csf2) identified as a top-ranked upstream driver and inflammatory mediator associated with recovery of homeostasis. Early growth response (Egr1), C-C motif chemokine ligand 8 (Ccl8), and Collagen, type V, alpha 1 (Col5a1) were also identified amongst the dysregulated genes. Additionally, acrylamide treatment led to subtle changes in the expression of genes that encode proteins secreted by the seminal vesicle, including the complement regulator, Complement factor b (Cfb). Conclusions These data add to emerging evidence demonstrating that the seminal vesicles, like other male reproductive tract tissues, are sensitive to environmental insults, and respond in a manner with potential to exert impact on fetal development and later offspring health.

scholarly journals Curcumin Protects the Seminal Vesicles from Metronidazole‑induced Reduction of Secretion in Mice

2012 ◽  
Vol 55 (1) ◽  
pp. 32-36 ◽  
Author(s):  
Ali Noorafshan ◽  
Saied Karbalay‑Doust
Keyword(s):  
Body Weight ◽  
Seminal Vesicle ◽  
Structural Changes ◽  
Reproductive Tract ◽  
Anaerobic Bacteria ◽  
Seminal Vesicles ◽  
Female Reproductive Tract ◽  
Sperm Chromatin ◽  
Control Group ◽  
Negative Effects

Seminal vesicle secretion is important for increasing the stability of sperm chromatin, inhibition of the immune activity in the female reproductive tract and so on. Metronidazole (MTZ), a drug used for treatment of infections caused by anaerobic bacteria and protozoa, may have negative effects on the genital gland including the seminal vesicles. Curcumin exhibits antioxidant as well as anti‑inflammatory properties. The present study aims to evaluate the negative effects of MTZ on the seminal vesicle structure and ameliorative effects of curcumin using stereological methods. Thirty balb/c mice were divided into six groups. The control group was received distilled water. The second and the third received higher doses of MTZ (500 mg/kg body weight/day) and MTZ (500 mg/kg/day) + 100 mg/kg/day curcumin, respectively. The fourth and the fifth were treated with lower doses of MTZ (165 mg/kg body weight/day) and MTZ (165 mg/kg body weight/day) + curcumin (100 mg/kg body weight/day), respectively. The sixth group received 100 mg/kg body weight/day curcumin. All the administrations were done by oral gavages for 14 days. After 30 days, seminal vesicles were removed. Stereological study of the seminal vesicle structure revealed a significant reduction in gland and vesicular fluid volume in MTZ‑treated (higher or lower doses) animals. Curcumin protected the reduction of both parameters in therapeutic‑dose treated animals. Metronidazole treatment does not induce structural changes in the seminal gland; however, it can have a significant impact on its secretion ability. Importantly, these deteriorations might be preventable by curcumin co‑treatment.

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

Reproduction ◽  
2016 ◽  
Vol 152 (4) ◽  
pp. 313-321 ◽  
Author(s):  
Naoya Araki ◽  
Natsuko Kawano ◽  
Woojin Kang ◽  
Kenji Miyado ◽  
Kaoru Yoshida ◽  
...  
Keyword(s):  
Seminal Vesicle ◽  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
The Other ◽  
Sperm Capacitation ◽  
Other Hand ◽  
Sperm Membrane ◽  
Vesicle Secretion ◽  
Mammalian Spermatozoa

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 forin vivofertilization. However, the effects of SVSs other than SVS2 on the sperm have not been elucidated. Since mouseSvs2–Svs6genes 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.

scholarly journals The Concept of Male Reproductive Anatomy

2021 ◽  
Author(s):  
Oyovwi Mega Obukohwo ◽  
Nwangwa Eze Kingsley ◽  
Rotu Arientare Rume ◽  
Emojevwe Victor
Keyword(s):  
Reproductive System ◽  
Reproductive Tract ◽  
Prostate Gland ◽  
Ejaculatory Duct ◽  
Seminal Vesicles ◽  
Female Reproductive Tract ◽  
Male Reproductive System ◽  
Male Gametes ◽  
Human Reproductive ◽  
Reproductive Anatomy

The human reproductive system is made up of the primary and secondary organs, which helps to enhances reproduction. The male reproductive system is designed to produce male gametes and convey them to the female reproductive tract through the use of supportive fluids and testosterone synthesis. The paired testis (site of testosterone and sperm generation), scrotum (compartment for testis localisation), epididymis, vas deferens, seminal vesicles, prostate gland, bulbourethral gland, ejaculatory duct, urethra, and penis are the parts of the male reproductive system. The auxiliary organs aid in the maturation and transportation of sperm. Semen is made up of sperm and the secretions of the seminal vesicles, prostate, and bulbourethral glands (the ejaculate). Ejaculate is delivered to the female reproduc¬tive tract by the penis and urethra. The anatomy, embryology and functions of the male reproductive system are discussed in this chapter.

scholarly journals Does the Act of Copulation per se, without Considering Seminal Deposition, Change the Expression of Genes in the Porcine Female Genital Tract?

2020 ◽  
Vol 21 (15) ◽  
pp. 5477
Author(s):  
Manuel Alvarez-Rodriguez ◽  
Cristina A. Martinez ◽  
Dominic Wright ◽  
Heriberto Rodriguez-Martinez
Keyword(s):  
Gene Expression ◽  
Genital Tract ◽  
Reproductive Tract ◽  
Female Genital Tract ◽  
Female Reproductive Tract ◽  
Smooth Muscle Contractility ◽  
Expression Of Genes ◽  
Per Se ◽  
Natural Mating ◽  
Transcriptomic Changes

Semen—through its specific sperm and seminal plasma (SP) constituents—induces changes of gene expression in the internal genital tract of pigs, particularly in the functional sperm reservoir at the utero-tubal junction (UTJ). Although seminal effects are similarly elicited by artificial insemination (AI), major changes in gene expression are registered after natural mating, a fact suggesting the act of copulation induces per se changes in genes that AI does not affect. The present study explored which pathways were solely influenced by copulation, affecting the differential expression of genes (DEGs) of the pre/peri-ovulatory genital tract (cervix, distal uterus, proximal uterus and UTJ) of estrus sows, 24 h after various procedures were performed to compare natural mating with AI of semen (control 1), sperm-free SP harvested from the sperm-peak fraction (control 2), sperm-free SP harvested from the whole ejaculate (control 3) or saline-extender BTS (control 4), using a microarray chip (GeneChip® porcine gene 1.0 st array). Genes related to neuroendocrine responses (ADRA1, ADRA2, GABRB2, CACNB2), smooth muscle contractility (WNT7A), angiogenesis and vascular remodeling (poFUT1, NTN4) were, among others, overrepresented with distal and proximal uterine segments exhibiting the highest number of DEGs. The findings provide novel evidence that relevant transcriptomic changes in the porcine female reproductive tract occur in direct response to the specific act of copulation, being semen-independent.

scholarly journals Alterations in egg white-related genes expression in response to hormonal stimulation

Reproduction ◽  
2020 ◽  
Vol 160 (5) ◽  
pp. 793-801
Author(s):  
Minkyeong Lee ◽  
Changwon Yang ◽  
Gwonhwa Song ◽  
Whasun Lim
Keyword(s):  
Reproductive System ◽  
Hormonal Regulation ◽  
Egg Production ◽  
Reproductive Tract ◽  
Egg White ◽  
Female Reproductive Tract ◽  
Expression Of Genes ◽  
Egg White Proteins ◽  
Study Results ◽  
Genes Encoding

The reproductive tract in avian females is sensitive to hormonal regulation. Exogenous estrogen induces immature oviduct development to improve egg production after molting. In this process, regressed female reproductive tract is regenerated in response to the secretion of estrogen. However, there is limited knowledge on the physiological mechanisms underlying the regulation of the avian female reproductive system. In our previous study, results from microarray analysis revealed that the expression of genes encoding egg white proteins is affected during molting. Herein, we artificially induced the molting period in chickens through a zinc-containing diet. Subsequently, changes in the expression of genes encoding egg white proteins were confirmed in the oviduct tissue. The levels of MUC5B, ORM1, RTBDN, and TENP mRNA were significantly high in the oviduct, and the genes were repressed in the regression phase, whereas these were expressed in the recrudescence phase, particularly in the luminal epithelium and glandular epithelium of the oviduct, during molting. Moreover, we observed that gene expression was induced in the magnum, the site for the secretion of egg white components. Next, differences in expression levels of the four genes in normal and cancerous ovaries were compared. Collectively, results suggest that the four selected genes are expressed in the female chicken reproductive tract in response to hormonal regulation, and egg white protein-encoding genes may serve as modulators of the reproductive system in hens.

scholarly journals Effects of colostrum, feeding method and oral IGF1 on porcine uterine development

Reproduction ◽  
2018 ◽  
Vol 155 (3) ◽  
pp. 259-271 ◽  
Author(s):  
Ashley F George ◽  
Kathleen M Rahman ◽  
Dori J Miller ◽  
Anne A Wiley ◽  
Meredith E Camp ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Reproductive Tract ◽  
Uterine Wall ◽  
Female Reproductive Tract ◽  
Milk Replacer ◽  
Endometrial Cell ◽  
Feeding Method ◽  
Oral Supplementation ◽  
Expression Of Genes ◽  
Uterine Development

Nursing ensures lactocrine delivery of maternally derived, milk-borne bioactive factors to offspring, which affects postnatal development of female reproductive tract tissues. Disruption of lactocrine communication for two days from birth (postnatal day (PND) 0) by feeding milk replacer in lieu of nursing or consumption of colostrum alters porcine uterine gene expression globally by PND 2 and inhibits uterine gland genesis by PND 14. Here, objectives were to determine effects of: (1) nursing or milk replacer feeding from birth; (2) a single dose of colostrum or milk replacer and method of feeding and (3) a single feeding of colostrum or milk replacer, with or without oral supplementation of IGF1, administered at birth on aspects of porcine uterine development at 12-h postnatally. Results indicate nursing for 12 h from birth supports rapid establishment of a uterine developmental program, illustrated by patterns of endometrial cell proliferation, expression of genes associated with uterine wall development and entry into mitosis and establishment of a uterine MMP9/TIMP1 system. A single feeding of colostrum at birth increased endometrial cell proliferation at 12 h, regardless of method of feeding. Oral supplementation of IGF1 was sufficient to support endometrial cell proliferation at 12 h in replacer-fed gilts, and supplementation of colostrum with IGF1 further increased endometrial cell proliferation. Results indicate that lactocrine regulation of postnatal uterine development is initiated with the first ingestion of colostrum. Further, results suggest IGF1 may be lactocrine-active and support a 12-h bioassay, which can be used to identify uterotrophic lactocrine activity.

Prostatic growth and development are regulated by FGF10

Development ◽  
1999 ◽  
Vol 126 (16) ◽  
pp. 3693-3701
Author(s):  
A.A. Thomson ◽  
G.R. Cunha
Keyword(s):  
Organ Culture ◽  
Seminal Vesicle ◽  
Growth And Development ◽  
Reproductive Tract ◽  
Mesenchymal Cells ◽  
Female Reproductive Tract ◽  
Ventral Prostate ◽  
Serum Free

We have examined the role of Fibroblast Growth Factor 10 (FGF10) during the growth and development of the rat ventral prostate (VP) and seminal vesicle (SV). FGF10 transcripts were abundant at the earliest stages of organ formation and during neonatal organ growth, but were low or absent in growth-quiescent adult organs. In both the VP and SV, FGF10 transcripts were expressed only in a subset of mesenchymal cells and in a pattern consistent with a role as a paracrine epithelial regulator. In the neonatal VP, FGF10 mRNA was expressed initially in mesenchymal cells peripheral to the peri-urethral mesenchyme and distal to the elongating prostatic epithelial buds. At later stages, mesenchymal cells surrounding the epithelial buds also expressed FGF10 transcripts. During induction of the SV, FGF10 mRNA was present in mesenchyme surrounding the lower Wolffian ducts and, at later stages, FGF10 transcripts became restricted to mesenchymal cells subadjacent to the serosa. We investigated whether the FGF10 gene might be regulated by androgens by analysing the levels of FGF10 transcripts in SV and VP organs grown in serum-free organ culture. While FGF10 transcript levels increased after treatment with testosterone in the SV (but not VP), these changes were not sensitive to anti-androgen treatment, and thus it is likely that FGF10 mRNA was not directly regulated by testosterone. Also, FGF10 mRNA was observed in the embryonic female reproductive tract in a position analogous to that of the ventral prostate in males suggesting that FGF10 is not regulated by androgens in vivo. Recombinant FGF10 protein specifically stimulated growth of Dunning epithelial and BPH1 prostatic epithelial cell lines, but had no effect on growth of Dunning stromal cells or primary SV mesenchyme. Furthermore, FGF10 protein stimulated the development of ventral prostate and seminal vesicle organ rudiments in serum-free organ culture. When both FGF10 and testosterone were added to organs in vitro, there was no synergistic induction of development. Additionally, development induced by FGF10 was not inhibited by the addition of the anti-androgen Cyproterone Acetate demonstrating that the effects of FGF10 were not mediated by the androgen receptor. Taken together, our experiments suggest that FGF10 functions as a mesenchymal paracrine regulator of epithelial growth in the prostate and seminal vesicle and that the FGF10 gene is not regulated by androgens

287. LPS introduced at mating induces KC production in the murine uterus during early pregnancy

2005 ◽  
Vol 17 (9) ◽  
pp. 121
Author(s):  
D. J. Glynn ◽  
S. A. Robertson
Keyword(s):  
Seminal Vesicle ◽  
Seminal Plasma ◽  
Early Pregnancy ◽  
Reproductive Tract ◽  
Seminal Fluid ◽  
Female Reproductive Tract ◽  
Tissue Remodelling ◽  
Uterine Epithelial Cell ◽  
Female Mice ◽  
Vesicle Fluid

An inflammatory cascade is elicited in the female reproductive tract following mating in mice. The recruited leukocytes and cytokines have roles in facilitating implantation through activating immunological tolerance and endometrial tissue remodelling. We have previously shown that seminal plasma acts to induce synthesis of GM-CSF and IL-6 in the female reproductive tract in response to TGFβ1 present in seminal fluid. Recently we have shown that chemokines, specifically the neutrophil chemoattractant KC, is dramatically upregulated after mating. The purpose of this study was to identify the active constituent of semen responsible for KC induction. Female mice were mated with either intact, seminal vesicle deficient or vasectomized males and uterine flushings were collected approximately 8 h later, when KC content was measured by specific ELISA. KC production was increased 13-fold, 6-fold and 10-fold respectively, indicating that neither the seminal plasma nor the sperm fraction of semen was necessary for induction. To investigate more precisely the identity of the KC inducing factor, an in vitro primary uterine epithelial cell culture system was employed. Uterine epithelial cells were harvested from estrous female mice and exposed to a range of doses of seminal vesicle fluid, TGFβ1or lipopolysaccharide (LPS). Following addition of seminal vesicle fluid or TGFβ1 KC production was decreased by 100% and 58% respectively whereas it was increased ~2-fold in response to LPS. Together these data indicate that LPS derived from the male or lower female reproductive tract accessing the uterus after insemination is required for KC induction, and implicate commensal bacteria as having a key regulatory role in the cellular and molecular quality of the uterine immune environment during early pregnancy.

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