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, E.; Matte, A.; Ghigo, A.; Andolfo, I.; James, C.; Siciliano, A.; Leboeuf, C.; Janin, A.; Manna, F.; Choi, S. Y.; Iolascon, A.; Beneduce, E.; Melisi, D.; Kim, D. W.; Levi, S.; De Franceschi, L.. - 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
Levi S.Membro del Collaboration Group
;
2017-01-01
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.
