title: Cellular bioenergetics changes in magnocellular neurons may affect copeptin expression in the late phase of sepsis.
abstract: We investigated whether inflammatory mediators during cecal ligation and puncture (CLP)-induced sepsis may diminish copeptin expression in magnocellular neurons, thus affecting arginine-vasopressin (AVP) synthesis. The transcript abundance of IL-1β, IL-1R1, iNOS and HIF-1α was continuously elevated. IL-1β, iNOS and cytochrome c protein levels progressively increased until 24h. Immunostaining for these proteins was higher at 6 and 24h, as also seen in the annexin-V assay, while copeptin was continuously decreased. This suggests that increased IL-1β and NO levels may cause significant bioenergetics changes in magnocellular neurons, affecting copeptin expression and compromising AVP synthesis and secretion in the late phase of sepsis.
authors.affiliation: Departamento de Morfologia, Fisiologia e Patologia Básica, Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil. Electronic address: gabi.pelegrin@gmail.com.
authors.forename: Gabriela R
authors.initials: GR
authors.lastname: Oliveira-Pelegrin
authors.affiliation: Departamento de Morfologia, Fisiologia e Patologia Básica, Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Paulo J
authors.initials: PJ
authors.lastname: Basso
authors.affiliation: Departamento de Morfologia, Fisiologia e Patologia Básica, Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Maria José A
authors.initials: MJ
authors.lastname: Rocha
mesh_terms: D000818:Animals; D017304:Annexin A5 / Q000378:metabolism; D001127:Arginine Vasopressin / Q000235:genetics / Q000378:metabolism; D002432:Cecum; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology*; D006020:Glycopeptides / Q000378:metabolism*; D007031:Hypothalamus / Q000473:pathology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D009897:Optic Chiasm / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D053573:Receptors, Interleukin-1 Type I / Q000235:genetics / Q000378:metabolism; D018805:Sepsis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D017304:Annexin A5; D006020:Glycopeptides; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D012333:RNA, Messenger; D053573:Receptors, Interleukin-1 Type I; C048197:copeptins; D001127:Arginine Vasopressin; D052247:Nitric Oxide Synthase Type II
keywords: Apoptosis; Hypoxia-induced factor-1α; Interleukin-1β; Nitric oxide synthase; Oxidative stress; Supraoptic nucleus