title: NF-κB involvement in hyperoxia-induced myocardial damage in newborn rat hearts.
abstract: Premature newborns are frequently exposed to hyperoxia ventilation and some literature data indicate the possibility of hyperoxia-induced myocardial damage. Since nuclear factor κB (NF-κB) is a crucial signaling molecule involved in physiological response to hyperoxia in different cell types as well as in various tissues, our attention has been focused on the role played by NF-κB pathway in response to moderate and severe hyperoxia exposure in rat neonatal heart tissue. Akt and IκBα levels, involved in NF-κB activation, along with the balance between apoptotic and survival pathways have also been investigated. Experimental design of the study has involved exposure of newborn rats to room air (controls), 60 % O2 (moderate hyperoxia), or 95 % O2 (severe hyperoxia) for the first two postnatal weeks. Morphological analysis shows a less compact tissue in rat heart exposed to moderate hyperoxia and a decreased number of nuclei in samples exposed to severe hyperoxia. A significant increase of NF-κB positive nuclei percentage and p-IκBα expression in samples exposed to 95 % hyperoxia compared to control and to 60 % hyperoxia is evidenced; in parallel, an increase of pAkt/Akt ratio in both samples exposed to 95 and 60 % hyperoxia is shown. Furthermore, a more evident cytochrome c/Apaf-1 immunocomplex and a decreased Bcl2 expression in 95 % hyperoxia-exposed sample compared to 60 % exposed one is evidenced. In conclusion, our findings suggest the involvement of the NF-κB pathway and Akt signaling in the mechanisms of myocardial hyperoxic damage in the newborns, with particular reference to the induction of oxidative stress-related apoptosis.
authors.affiliation: Section of Human Anatomy, Department of Pharmacy, University "G. d'Annunzio" Chieti-Pescara, Chieti, Italy, s.zara@unich.it.
authors.forename: Susi
authors.initials: S
authors.lastname: Zara
authors.forename: Marianna
authors.initials: M
authors.lastname: De Colli
authors.forename: Monica
authors.initials: M
authors.lastname: Rapino
authors.forename: Valentina
authors.initials: V
authors.lastname: Di Valerio
authors.forename: Guya Diletta
authors.initials: GD
authors.lastname: Marconi
authors.forename: Amelia
authors.initials: A
authors.lastname: Cataldi
authors.forename: Veronica
authors.initials: V
authors.lastname: Macchi
authors.forename: Raffaele
authors.initials: R
authors.lastname: De Caro
authors.forename: Andrea
authors.initials: A
authors.lastname: Porzionato
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis; D004195:Disease Models, Animal; D005260:Female; D006321:Heart; D018496:Hyperoxia / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism*; D018384:Oxidative Stress; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction
chemical_list: D016328:NF-kappa B; D051057:Proto-Oncogene Proteins c-akt