Inhibition of pre-B cell colony-enhancing factor attenuates inflammation induced by hyperoxia in EA.hy926 cells

He, Jiawei; Cui, Huan Jin; Tang, Li; Chen, Jinwen; Huang, Wei

doi:10.3892/ijmm.2017.3045

Cited by 2 publications

(1 citation statement)

References 48 publications

(49 reference statements)

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“…These data are in line with the suggestion from the same group that hyperoxia disrupted ERK1/2 signaling and ERK1/2-dependent angiogenesis in vitro (378). The silencing of nicotinamide phosphoribosyltransferase (NAMPT, also called pre-B cell colony-enhancing factor), using an siRNA approach, attenuated proinflammatory effects of hyperoxia in EA.hy9286 cells (an umbilical vein endothelial cell-derived cell-line) (201).…”

Section: New Interventional Strategies To Drive Alveolarizationsupporting

confidence: 88%

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Lignelli

Palumbo

Myti

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

109

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Bronchopulmonary dysplasia (BPD) is the most common cause of morbidity and mortality in preterm infants. A key histopathological feature of BPD is stunted late lung development, where the process of alveolarization—the generation of alveolar gas exchange units—is impeded, through mechanisms that remain largely unclear. As such, there is interest in the clarification both of the pathomechanisms at play in affected lungs, and the mechanisms of de novo alveoli generation in healthy, developing lungs. A better understanding of normal and pathological alveolarization might reveal opportunities for improved medical management of affected infants. Furthermore, disturbances to the alveolar architecture are a key histopathological feature of several adult chronic lung diseases, including emphysema and fibrosis, and it is envisaged that knowledge about the mechanisms of alveologenesis might facilitate regeneration of healthy lung parenchyma in affected patients. To this end, recent efforts have interrogated clinical data, developed new—and refined existing—in vivo and in vitro models of BPD, have applied new microscopic and radiographic approaches, and have developed advanced cell-culture approaches, including organoid generation. Advances have also been made in the development of other methodologies, including single-cell analysis, metabolomics, lipidomics, and proteomics, as well as the generation and use of complex mouse genetics tools. The objective of this review is to present advances made in our understanding of the mechanisms of lung alveolarization and BPD over the period 1 January 2017–30 June 2019, a period that spans the 50th anniversary of the original clinical description of BPD in preterm infants.

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Section: New Interventional Strategies To Drive Alveolarizationsupporting

confidence: 88%

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Lignelli

Palumbo

Myti

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

109

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Effects of genistein on lipopolysaccharide-induced injury of mouse alveolar epithelial cells and its mechanism

Zhu

Zhang

et al. 2020

Bioscience, Biotechnology, and Biochemistry

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Alveolar and bronchial epithelial cells have critical functions in acute respiratory distress syndrome progress. Genistein could protect the lungs from acute lung injury, however, whether genistein protects the alveolar epithelial cells from LPS-induced injury was less studied. Spectrophotometric method 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and enzyme-linked immunosorbent assay (ELISA) were performed to detect cell viability and levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Flow cytometry and western blot assay were performed to detect cells apoptosis and protein levels. In LPS-induced model of mouse lung epithelial (MLE)-12 cells, PBEF (proinflammatory cytokine) expression, and cell apoptosis were increased and cell viability was decreased, whereas NF-κB was activated and expression levels of TNF-α, IL-1β, and IL-6 were increased. However, genistein partly reversed the effect of LPS, and it plays a protective role in lung injury by reducing expression of PBEF, inhibiting the activation of NF-κB and alleviating inflammatory response of cells.

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Inhibition of pre-B cell colony-enhancing factor attenuates inflammation induced by hyperoxia in EA.hy926 cells

Cited by 2 publications

References 48 publications

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Effects of genistein on lipopolysaccharide-induced injury of mouse alveolar epithelial cells and its mechanism

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