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Article: Intermedin attenuates LPS-induced inflammation in the rat testis

TitleIntermedin attenuates LPS-induced inflammation in the rat testis
Authors
Issue Date2013
Citation
PLOS ONE, 2013, v. 8 n. 6, p. e65278 How to Cite?
AbstractFirst reported as a vasoactive peptide in the cardiovascular system, intermedin (IMD), also known as adrenomedullin 2 (ADM2), is a hormone with multiple potent roles, including its antioxidant action on the pulmonary, central nervous, cardiovascular and renal systems. Though IMD may play certain roles in trophoblast cell invasion, early embryonic development and cumulus cell-oocyte interaction, the role of IMD in the male reproductive system has yet to be investigated. This paper reports our findings on the gene expression of IMD, its receptor components and its protein localization in the testes. In a rat model, bacterial lippolysaccharide (LPS) induced atypical orchitis, and LPS treatment upregulated the expression of IMD and one of its receptor component proteins, i.e. receptor activity modifying protein 2 (RAMP2). IMD decreased both plasma and testicular levels of reactive oxygen species (ROS) production, attenuated the increase in the gene expression of the proinflammatory cytokines tumor necrosis factor alpha (TNFα), interleukin 6 (IL6) and interleukin 1 beta (IL1β), rescued spermatogenesis, and prevented the decrease in plasma testosterone levels caused by LPS. The restorative effect of IMD on steroidogenesis was also observed in hydrogen peroxide-treated rat primary Leydig cells culture. Our results indicate IMD plays an important protective role in spermatogenesis and steroidogenesis, suggesting therapeutic potential for IMD in pathological conditions such as orchitis.
Persistent Identifierhttp://hdl.handle.net/10722/184455
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLi, Len_US
dc.contributor.authorMa, Pen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorHuang, Cen_US
dc.contributor.authorO, WSen_US
dc.contributor.authorTang, Fen_US
dc.contributor.authorZhang, JVen_US
dc.date.accessioned2013-07-15T09:47:25Z-
dc.date.available2013-07-15T09:47:25Z-
dc.date.issued2013en_US
dc.identifier.citationPLOS ONE, 2013, v. 8 n. 6, p. e65278en_US
dc.identifier.urihttp://hdl.handle.net/10722/184455-
dc.description.abstractFirst reported as a vasoactive peptide in the cardiovascular system, intermedin (IMD), also known as adrenomedullin 2 (ADM2), is a hormone with multiple potent roles, including its antioxidant action on the pulmonary, central nervous, cardiovascular and renal systems. Though IMD may play certain roles in trophoblast cell invasion, early embryonic development and cumulus cell-oocyte interaction, the role of IMD in the male reproductive system has yet to be investigated. This paper reports our findings on the gene expression of IMD, its receptor components and its protein localization in the testes. In a rat model, bacterial lippolysaccharide (LPS) induced atypical orchitis, and LPS treatment upregulated the expression of IMD and one of its receptor component proteins, i.e. receptor activity modifying protein 2 (RAMP2). IMD decreased both plasma and testicular levels of reactive oxygen species (ROS) production, attenuated the increase in the gene expression of the proinflammatory cytokines tumor necrosis factor alpha (TNFα), interleukin 6 (IL6) and interleukin 1 beta (IL1β), rescued spermatogenesis, and prevented the decrease in plasma testosterone levels caused by LPS. The restorative effect of IMD on steroidogenesis was also observed in hydrogen peroxide-treated rat primary Leydig cells culture. Our results indicate IMD plays an important protective role in spermatogenesis and steroidogenesis, suggesting therapeutic potential for IMD in pathological conditions such as orchitis.-
dc.languageengen_US
dc.relation.ispartofPLOS ONEen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleIntermedin attenuates LPS-induced inflammation in the rat testisen_US
dc.typeArticleen_US
dc.identifier.emailO, WS: owaisum@hkucc.hku.hken_US
dc.identifier.emailTang, F: ftang@hkucc.hku.hken_US
dc.identifier.authorityO, WS=rp00315en_US
dc.identifier.authorityTang, F=rp00327en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0065278-
dc.identifier.pmcidPMC3672160-
dc.identifier.hkuros215584en_US
dc.identifier.volume8en_US
dc.identifier.issue6en_US
dc.identifier.spagee65278en_US
dc.identifier.epagee65278en_US

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