The data presented in this article are related to the research paper entitled “peroxiredoxin-2 plays a pivotal role as multimodal cytoprotector in the early phase of pulmonary hypertension” (Federti et al., 2017) [1]. Data show that the absence of peroxiredoxin-2 (Prx2) is associated with increased lung oxidation and pulmonary vascular endothelial dysfunction. Prx2−/− mice displayed activation of the redox-sensitive transcriptional factors, NF-kB and Nrf2, and increased expression of cytoprotective system such as heme-oxygenase-1 (HO-1). We also noted increased expression of both markers of vascular activation and extracellular matrix remodeling. The administration of the recombinant fusion protein PEP Prx2 reduced the activation of NF-kB and Nrf2 and was paralleled by a decrease in HO-1 and in vascular endothelial abnormal activation. Prolonged hypoxia was used to trigger pulmonary artery hypertension (PAH). Prx2−/− precociously developed PAH compared to wildtype animals.

Data demonstrating the role of peroxiredoxin 2 as important anti-oxidant system in lung homeostasis

Ghigo, Alessandra;James, Cimino;LEVI, Sonia Maria Rosa;De Franceschi, Lucia
2017

Abstract

The data presented in this article are related to the research paper entitled “peroxiredoxin-2 plays a pivotal role as multimodal cytoprotector in the early phase of pulmonary hypertension” (Federti et al., 2017) [1]. Data show that the absence of peroxiredoxin-2 (Prx2) is associated with increased lung oxidation and pulmonary vascular endothelial dysfunction. Prx2−/− mice displayed activation of the redox-sensitive transcriptional factors, NF-kB and Nrf2, and increased expression of cytoprotective system such as heme-oxygenase-1 (HO-1). We also noted increased expression of both markers of vascular activation and extracellular matrix remodeling. The administration of the recombinant fusion protein PEP Prx2 reduced the activation of NF-kB and Nrf2 and was paralleled by a decrease in HO-1 and in vascular endothelial abnormal activation. Prolonged hypoxia was used to trigger pulmonary artery hypertension (PAH). Prx2−/− precociously developed PAH compared to wildtype animals.
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Multidisciplinary
Federti, Enrica; Matte, Alessandro; Ghigo, Alessandra; Andolfo, Immacolata; James, Cimino; Siciliano, Angela; Leboeuf, Christophe; Janin, Anne; Manna, Francesco; Choi, Soo Young; Iolascon, Achille; Beneduce, Elisabetta; Melisi, Davide; Kim, Dae Won; Levi, Sonia; De Franceschi, Lucia*
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/1662293
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