Transcriptomic analysis of the seminal vesicle response to the reproductive toxicant acrylamide.


Journal

BMC genomics
ISSN: 1471-2164
Titre abrégé: BMC Genomics
Pays: England
ID NLM: 100965258

Informations de publication

Date de publication:
08 Oct 2021
Historique:
received: 26 02 2021
accepted: 14 08 2021
entrez: 9 10 2021
pubmed: 10 10 2021
medline: 13 10 2021
Statut: epublish

Résumé

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. 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). 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.

Sections du résumé

BACKGROUND 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 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 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.

Identifiants

pubmed: 34625024
doi: 10.1186/s12864-021-07951-1
pii: 10.1186/s12864-021-07951-1
pmc: PMC8499523
doi:

Substances chimiques

Cytokines 0
Acrylamide 20R035KLCI

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

728

Informations de copyright

© 2021. The Author(s).

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Auteurs

David A Skerrett-Byrne (DA)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Brett Nixon (B)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Elizabeth G Bromfield (EG)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.
Department of Biochemistry and Cell Biology, Faculty of Veterinary Medicine, Utrecht University, 3584 CM, Utrecht, The Netherlands.

James Breen (J)

The Robinson Research Institute and Adelaide Medical School, University of Adelaide, Adelaide, SA, 5005, Australia.
South Australian Genomics Centre (SAGC), South Australian Health & Medical Research Institute (SAHMRI), Adelaide, SA, 5000, Australia.
Computational & Systems Biology Program, Precision Medicine Theme, South Australian Health & Medical Research Institute (SAHMRI), Adelaide, SA, 5000, Australia.
Adelaide Medical School, Faculty of Health & Medical Sciences, University of Adelaide, Adelaide, SA, 5005, Australia.

Natalie A Trigg (NA)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Simone J Stanger (SJ)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Ilana R Bernstein (IR)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Amanda L Anderson (AL)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Tessa Lord (T)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

R John Aitken (RJ)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Shaun D Roman (SD)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia.

Sarah A Robertson (SA)

The Robinson Research Institute and Adelaide Medical School, University of Adelaide, Adelaide, SA, 5005, Australia.
Adelaide Medical School, Faculty of Health & Medical Sciences, University of Adelaide, Adelaide, SA, 5005, Australia.

John E Schjenken (JE)

Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, Discipline of Biological Sciences, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia. john.schjenken@newcastle.edu.au.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW, 2305, Australia. john.schjenken@newcastle.edu.au.

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