Effect of Short-term Exposure of Different Concentrations of Hyperoxia on Fetal Alveolar Type II Cell Death

Lee, Hyeon Soo

doi:10.5385/nm.2013.20.2.199

Cited by 3 publications

(4 citation statements)

References 28 publications

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“…This could play an important role in the evolution of ‘new’ BPD from an early postnatal age in preterm infants . Previous observations from our laboratory also support this idea by showing that hyperoxia‐induced type II cell injury including cellular necrosis begins from a very early stage of hyperoxia (<12 hrs) . Considering these evidence, it is highly suggested to pay closer attention to minimizing lung injury, especially type II cell injury starting in the early postnatal stage in preterm newborns.…”

Section: Introductionsupporting

confidence: 67%

“…Considering these evidence, it is highly suggested to pay closer attention to minimizing lung injury, especially type II cell injury starting in the early postnatal stage in preterm newborns. However, unfortunately, there are no specific measures for the protection of preterm lungs against injury induced from a very early stage (<6 hrs) of hyperoxia .…”

Section: Introductionmentioning

confidence: 99%

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rIL‐10 enhances IL‐10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia

Lee

2015

J Cellular Molecular Medi

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Although the mechanisms by which hyperoxia promotes bronchopulmonary dysplasia are not fully defined, the inability to maintain optimal interleukin (IL)-10 levels in response to injury secondary to hyperoxia seems to play an important role. We previously defined that hyperoxia decreased IL-10 production and pre-treatment with recombinant IL-10 (rIL-10) protected these cells from injury. The objectives of these studies were to investigate the responses of IL-10 receptors (IL-10Rs) and IL-10 signalling proteins (IL-10SPs) in hyperoxic foetal alveolar type II cells (FATIICs) with and without rIL-10. FATIICs were isolated on embryonic day 19 and exposed to 65%-oxygen for 24 hrs. Cells in room air were used as controls. IL-10Rs protein and mRNA were analysed by ELISA and qRT-PCR, respectively. IL-10SPs were assessed by Western blot using phospho-specific antibodies. IL-10Rs protein and mRNA increased significantly in FATIICs during hyperoxia, but JAK1 and TYK2 phosphorylation showed the opposite pattern. To evaluate the impact of IL-8 (shown previously to be increased) and the role of IL-10Rs, IL-10SPs were reanalysed in IL-8-added normoxic cells and in the IL-10Rs’ siRNA-treated hyperoxic cells. The IL-10Rs’ siRNA-treated hyperoxic cells and IL-8-added normoxic cells showed the same pattern in IL10SPs with the hyproxic cells. And pre-treatment with rIL-10 prior to hyperoxia exposure increased phosphorylated IL-10SPs, compared to the rIL-10-untreated hyperoxic cells. These studies suggest that JAK1 and TYK2 were significantly suppressed during hyperoxia, where IL-8 may play a role, and rIL-10 may have an effect on reverting the suppressed JAK1 and TYK2 in FATIICs exposed to hyperoxia.

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Section: Introductionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

rIL‐10 enhances IL‐10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia

Lee

2015

J Cellular Molecular Medi

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Section: Death Responses Of Fatiics During the Acute Stage Of Hyperox...mentioning

confidence: 66%

“…According to our previous observations, FATIICs generally show a necrotic aspect during the acute stage of hyperoxia rather than apoptosis 24) . Our laboratory investigated the response of fetal rat type II cell death following exposure to two different concentrations of hyperoxia (65%-and 85%-oxygen) for 36 h 24) . The pattern of fetal type II cell death analyzed by FACscan showed that hyperoxia causes significant increases in cellular necrosis in proportion to the oxygen-concentration and in a timedependent manner from the early stage of hyperoxia, from 6 h for 85%-oxygen and from 12 h for 65%-oxygen.…”

Section: Death Responses Of Fatiics During the Acute Stage Of Hyperox...mentioning

confidence: 66%

Fetal Alveolar Type II Cell Injury Induced by Short-term Exposure to Hyperoxia

Lee

2013

Neonatal Med

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A High concentration of oxygen (>40%) is used as a life-saving therapy in preterm newborns since birth. By generating excess reactive oxygen species, however, hy peroxia can cause lung injury leading to bronchopulmonary dysplasia (BPD). Although hyperoxia-induced lung injury contributes to the evolution of BPD, the mechanisms by which hyperoxia contributes to the genesis of lung injury in preterm lungs are not yet fully defined, and there are no specific measures for the protection of preterm lungs against injury secondary to hyperoxia. Alveolar type II cells are key components of the alveolar structure, and they are res ponsible for the restoration of normal alveolar epithelium after acute lung injury. However, hyperoxia is primarily delivered to the alveolar epithelium and alveolar type II cells can be the main target for the injury secondary to hyperoxia. To date, my researches have been focused on injury of fetal alveolar type II cells exposed to hyperoxia and the role of anti-inflammatory cytokine, IL-10 minimizing fetal type II cell injury induced by hyperoxia. Based on my previous studies, this article summarizes the cellular and molecular mechanisms of fetal type II cell injury induced in the early stage of hyperoxia and the protective potency of IL-10 in fetal alveolar type II cells and neonatal lungs injured by hyperoxia.

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Protective effect of recombinant interleukin-10 on newborn rat lungs exposed to short-term sublethal hyperoxia

Lee,

Ryu,

Lee

2024

Clin Exp Pediatr

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Background: Lung injury imposed by hyperoxia is the main cause of bronchopulmonary dysplasia in newborns. These injuries are generated from the early stage of hyperoxia through the main biologic effects of cell death and inflammatory response. Interleukin (IL)-10 is a potent anti-inflammatory cytokine that may have the inhibitory effects on these biologic actions induced by hyperoxia.Purpose: Based on our former in vitro studies investigating the effect of recombinant IL-10 (rIL-10) on protecting cultured alveolar type II cells exposed to short-term hyperoxia, we performed the in vivo study to investigate the effect of rIL-10 in newborn rats aged P4 exposed to hyperoxia.Methods: Rats were classified into 3 groups; the control group exposed to normoxia for 24 hours; the hyperoxia group exposed to 65% hyperoxia for 24 hours; and the IL10 group treated with intratracheal instillation of rIL-10 prior to exposure to 65% hyperoxia for 24 hours. Following each treatment, the rats were euthanized. Individual lobes of the right lung were prepared for hematoxyling and eosin (H&E) staining and immunohistochemical staining for thyroid transcription factor-1 (TTF1). Bronchoalveolar lavage (BAL) was performed in the left lung to analyze cell counts and cytokines.Results: The IL10 group showed preserved air spaces similar to the control group, with decreased cellularity compared to the hyperoxia group, whereas the hyperoxia group showed markedly reduced air spaces with increased cellularity compared to the IL10 group. And, the IL10 group showed more TTF1-positive cells, which represented alveolar type II cells, compared to the hyperoxia group. Inflammatory cells, such as neutrophils and lymphocytes and proinflammatory cytokines of tumor necrosis factor-α, IL-1α, IL-8, and macrophage inflammatory protein-1α were significantly lower in BAL fluid of the IL10 group compared to the hyperoxia group.Conclusion: These results indicate that rIL-10 may be a promising pharmaceutical measure for protecting newborn lungs from injury induced at the early stage of hyper oxia.

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Effect of Short-term Exposure of Different Concentrations of Hyperoxia on Fetal Alveolar Type II Cell Death

Cited by 3 publications

References 28 publications

rIL‐10 enhances IL‐10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia

rIL‐10 enhances IL‐10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia

Fetal Alveolar Type II Cell Injury Induced by Short-term Exposure to Hyperoxia

Protective effect of recombinant interleukin-10 on newborn rat lungs exposed to short-term sublethal hyperoxia

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