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Deactivation of the JNK Pathway by GSTP1 is essential to maintain sperm functionality

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dc.contributor.authorLlavanera, Marc
dc.contributor.authorMateo-Otero, Yentel
dc.contributor.authorDelgado-Bermúdez, Ariadna
dc.contributor.authorRecuero, Sandra
dc.contributor.authorOlives, Samuel
dc.contributor.authorBarranco Cascales, Isabel
dc.contributor.authorYeste, Marc
dc.contributor.departmentMedicina y Cirugía Animal
dc.contributor.otherFacultad de Veterinaria
dc.date.accessioned2025-10-17T10:11:02Z
dc.date.available2025-10-17T10:11:02Z
dc.date.copyright© 2021 Llavanera, Mateo-Otero, Delgado-Bermúdez, Recuero, Olives, Barranco and Yeste
dc.date.issued2021-02-25
dc.description.abstractFifty percent of male subfertility diagnosis is idiopathic and is usually associated with genetic abnormalities or protein dysfunction, which are not detectable through the conventional spermiogram. Glutathione S-transferases (GSTs) are antioxidant enzymes essential for preserving sperm function and maintaining fertilizing ability. However, while the role of GSTP1 in cell signaling regulation via the inhibition of c-Jun N-terminal kinases (JNK) has been enlightened in somatic cells, it has never been investigated in mammalian spermatozoa. In this regard, a comprehensive approach through immunoblotting, immunofluorescence, computer-assisted sperm assessment (CASA), and flow cytometry analysis was used to characterize the molecular role of the GSTP1-JNK heterocomplex in sperm physiology, using the pig as a model. Immunological assessments confirmed the presence and localization of GSTP1 in sperm cells. The pharmacological dissociation of the GSTP1-JNK heterocomplex resulted in the activation of JNK, which led to a significant decrease in sperm viability, motility, mitochondrial activity, and plasma membrane stability, as well as to an increase of intracellular superoxides. No effects in intracellular calcium levels and acrosome membrane integrity were observed. In conclusion, the present work has demonstrated, for the first time, the essential role of GSTP1 in deactivating JNK, which is crucial to maintain sperm function and has also set the grounds to understand the relevance of the GSTP1-JNK heterocomplex for the regulation of mammalian sperm physiology.
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dc.format.extent13
dc.identifier.citation Front. Cell Dev. Biol. 9:627140
dc.identifier.doihttps://doi.org/10.3389/fcell.2021.627140
dc.identifier.eissn2296-634X
dc.identifier.urihttp://hdl.handle.net/10201/167469
dc.languageeng
dc.publisherFrontiers Media
dc.relationThe authors acknowledged the support from the Ministry of Science, Innovation and Universities, Spain (RYC-2014-15581, AGL2017-88329-R, FJCI-2017-31689, and FPU18/00666), and Regional Government of Catalonia, Spain (2017-SGR-1229).The authors would like to thank the Technical Research Services (University of Girona) for their technical support. The authors would also like to thank the Servier Medical Art for their image bank used to create all figures.
dc.relation.publisherversionhttps://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.627140/full
dc.rightsAttribution 4.0 Internacional
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0
dc.subjectEzatiostat
dc.subjectGSTP1-JNK heterocomplex
dc.subjectMitochondria
dc.subjectSperm functionality
dc.subjectMammalian sperm
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleDeactivation of the JNK Pathway by GSTP1 is essential to maintain sperm functionality
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublicationes
relation.isAuthorOfPublication3c34d0d5-7d7d-4bcc-a119-8906f53baa7b
relation.isAuthorOfPublication.latestForDiscovery3c34d0d5-7d7d-4bcc-a119-8906f53baa7b
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