Knockdown of type 2 orexin receptor in adult mouse testis potentiates testosterone production and germ cell proliferation

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dc.contributor.authorSahoo P.
dc.contributor.authorSarkar D.
dc.contributor.authorSharma S.
dc.contributor.authorVerma A.
dc.contributor.authorNaik S.K.
dc.contributor.authorPrashar V.
dc.contributor.authorParkash J.
dc.contributor.authorSingh S.K.
dc.date.accessioned2025-01-13T07:03:42Z
dc.date.available2025-01-13T07:03:42Z
dc.date.issued2024
dc.description.abstractOrexins (OXs) are neuropeptides which regulate various physiological processes. OXs exist in two different forms, mainly orexin A (OXA) and orexin B (OXB) and their effects are mediated via OX1R and OX2R. Presence of OXB and OX2R in mouse testis is also reported. However, the role of OXB/OX2R in the male gonad remains unexplored. Herein we investigated the role of OXB/OX2R system in testicular physiology under in vivo and ex vivo conditions. Adult mice were given a single dose of bilateral intratesticular injection of siRNA targeting OX2R and were sacrificed 96 h post-injection. OX2R-knockdown potentiated serum and intratesticular testosterone levels with up-regulation in the expressions of major steroidogenic proteins. Germ cell proliferation also increased in siRNA-treated mice. Results of the ex vivo experiment also supported the findings of the in vivo study. In conclusion, OX2R may regulate testosterone production and thereby control the fine-tuning between steroidogenesis and germ cell dynamics. � 2024 Elsevier B.V.
dc.identifier.doi10.1016/j.mce.2024.112312
dc.identifier.issn3037207
dc.identifier.urihttps://dl.bhu.ac.in/ir/handle/123456789/1213
dc.language.isoen
dc.publisherElsevier Ireland Ltd
dc.subjectKnockdown
dc.subjectOX2R
dc.subjectOXB
dc.subjectSpermatogenesis
dc.subjectTestis
dc.subjectTestosterone
dc.titleKnockdown of type 2 orexin receptor in adult mouse testis potentiates testosterone production and germ cell proliferation
dc.typeArticle
journal.titleMolecular and Cellular Endocrinology
journalvolume.identifier.volume592

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