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 / 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. - In: DATA IN BRIEF. - ISSN 2352-3409. - 15:(2017), pp. 376-381. [10.1016/j.dib.2017.09.062]
Data demonstrating the role of peroxiredoxin 2 as important anti-oxidant system in lung homeostasis
Andolfo, Immacolata;Iolascon, Achille;
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.