Chronic Intermittent Hypoxia in Premature Infants: The Link Between Low Fat Stores, Adiponectin Receptor Signaling and Lung Injury

Kang, Na Young; Ivanovska, Julijana; Tamir-Hostovsky, Liran; Belik, Jaques; Gauda, Estelle B.

doi:10.1007/978-3-319-91137-3_19

Cited by 8 publications

(11 citation statements)

References 16 publications

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“…For the first time, we report the expression profile of APN and its receptors (AdipoR1 and AdipoR2) in specific cells in the lungs of newborn rats and show in an in vivo model the protective effects of rAPN against LPS-induced lung inflammation. Building on our previous data showing that mRNA and protein expression for APN and its receptors change from fetal day 19 to postnatal day 21 (Kang et al, 2018), we show that APN and its receptors (AdipoR1 and AdipoR2) are expressed in pulmonary fibroblasts, pulmonary epithelial cells, and PASMCs. In vitro, rAPN modified LPS-induced cytokine expression in PASMCs obtained from PND4 and PND7 rats.…”

Section: Discussionsupporting

confidence: 63%

“…At PND4, rat pups complete the saccular stage of lung development; between PND4 and PND7, alveolar density increases by threefold (Massaro, Teich, Maxwell, Massaro, & Whitney, 1985;Meyrick & Reid, 1982). While protein expression for APN, AdipoR1, and AdipoR2 in whole lung homogenates does not differ between PND4 and PND7 (Kang et al, 2018), we report here the differences in levels of these proteins in lung fibroblasts, epithelial cells, and PASMCs at these ages.…”

Section: Discussioncontrasting

confidence: 52%

“…We recently published the expression profile of lung APN, AdipoR1, and AdipoR2 in rats from fetal day 19 (FD19) to postnatal day 21 (PND21) (Kang, Ivanovska, Tamir-Hostovsky, Belik, & Gauda, 2018). In the current newborn rat study, the objectives were to describe the mRNA and protein expression profile of APN, AdipoR1, and AdipoR2 in lung cells and to characterize (a) the in vitro effect of rAPN on PASMC LPSinduced cytokine expression and (b) the cytokine and chemokine expression in lung homogenates, expression of immune cells in air spaces, and lung histology after aspiration of LPS in PND4 rats.…”

Section: Introductionmentioning

confidence: 99%

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Recombinant adiponectin protects the newborn rat lung from lipopolysaccharide‐induced inflammatory injury

et al. 2020

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Preterm infants are at high risk for developing bronchopulmonary dysplasia and pulmonary hypertension from inflammatory lung injury. In adult models, adiponectin (APN)—an adipocyte‐derived hormone—protects the lung from inflammatory injury and pulmonary vascular remodeling. Cord blood APN levels in premature infants born < 26 weeks gestation are 5% of the level in infants born at term. We previously reported the expression profile of APN and its receptors in neonatal rat lung homogenates during the first 3 weeks of postnatal development. Here, we characterize the expression profile of APN and its receptors in specific lung cells and the effects of exogenous recombinant APN (rAPN) on lipopolysaccharide‐(LPS)‐induced cytokine and chemokine production in total lung homogenates and specific lung cells. In vitro, rAPN added to primary cultures of pulmonary artery smooth muscle cells attenuated the expression of LPS‐induced pro‐inflammatory cytokines while increasing the expression of anti‐inflammatory cytokines. In vivo, intraperitoneal rAPN (2 mg/kg), given 4 hr prior to intrapharyngeal administration of LPS (5 mg/kg) to newborn rats at postnatal day 4, significantly reduced gene and protein expression of the pro‐inflammatory cytokine IL‐1ß and reduced protein expression of the chemokines monocyte chemoattractant protein (MCP‐1) and macrophage inflammatory protein‐1 alpha (MIP‐1α) in the lung. LPS‐induced histopathological changes in the lung were also decreased. Moreover, rAPN given 20 hr after intrapharyngeal LPS had a similar effect on lung inflammation. These findings suggest a role for APN in protecting the lung from inflammation during early stages of lung development.

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Section: Discussionsupporting

confidence: 63%

Section: Discussioncontrasting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

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Recombinant adiponectin protects the newborn rat lung from lipopolysaccharide‐induced inflammatory injury

et al. 2020

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“…Moreover, the chronic intermittent hypoxia in preterm neonates causes lung low-functional residual capacity and morbidity. 20 Both hypoxia and hyperoxia can produce and release a large number of oxygen-free radicals. Oxygen-free radicals are important causes of hypoxia-reoxygenation injury in cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of intermittent hypoxia or hyperoxia on lung development in preterm rat neonates during constant oxygen therapy

Wang

Zhang

et al. 2019

J of Cellular Biochemistry

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Impaired lung development is a major negative factor in the survival of preterm neonates. The present study was aimed to investigate the impact of constant oxygen, intermittent hyperoxia, and hypoxia on the lung development in preterm rat neonates. Neonatal rats were exposed to 40% O2 with or without brief hyperoxia episodes (95% O2) or brief hypoxia episodes (10% O2) from day 0 to day 14, or to room air. The body weight, radical alveolar count (RAC), and total antioxidant capacity (TAOC) were significantly lower whereas the lung coefficient and malondialdehyde (MDA) were significantly higher in the hyperoxia and hypoxia groups than the air control and constant oxygen group at day 7, day 14, and day 21 after birth. The lung function indexes were reduced by intermittent hyperoxia and hypoxia. In contrast, the constant oxygen therapy increased the lung function. HIF‐1α and VEGF expression were significantly increased by hypoxia and decreased by hyperoxia. The constant oxygen therapy only decreased the HIF‐1α expression at day 14 and 21. In summary, the constant oxygen treatment promoted lung function without affecting the antioxidative capacity in preterm rat neonates. While intermittent hyperoxia and hypoxia inhibited lung development, decreased antioxidative capacity, and dysregulated HIF‐1α/VEGF signaling in preterm rat neonates.

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“…The alveolar stage begins before birth and extends up to some years after birth [17,64,74]. Chronic hypoxia impairs alveolarization and lung development [7,75,76]. Pulmonary angiogenesis and secondary septation markedly increase the lung's surface area for gas exchange [17,27,64,77,78].…”

Section: Hypoxia and Vulnerability Of Neonatal Chronic Lung Diseasementioning

confidence: 99%

Intrauterine Hypoxia and Epigenetic Programming in Lung Development and Disease

et al. 2021

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Clinically, intrauterine hypoxia is the foremost cause of perinatal morbidity and developmental plasticity in the fetus and newborn infant. Under hypoxia, deviations occur in the lung cell epigenome. Epigenetic mechanisms (e.g., DNA methylation, histone modification, and miRNA expression) control phenotypic programming and are associated with physiological responses and the risk of developmental disorders, such as bronchopulmonary dysplasia. This developmental disorder is the most frequent chronic pulmonary complication in preterm labor. The pathogenesis of this disease involves many factors, including aberrant oxygen conditions and mechanical ventilation-mediated lung injury, infection/inflammation, and epigenetic/genetic risk factors. This review is focused on various aspects related to intrauterine hypoxia and epigenetic programming in lung development and disease, summarizes our current knowledge of hypoxia-induced epigenetic programming and discusses potential therapeutic interventions for lung disease.

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Chronic Intermittent Hypoxia in Premature Infants: The Link Between Low Fat Stores, Adiponectin Receptor Signaling and Lung Injury

Cited by 8 publications

References 16 publications

Recombinant adiponectin protects the newborn rat lung from lipopolysaccharide‐induced inflammatory injury

Recombinant adiponectin protects the newborn rat lung from lipopolysaccharide‐induced inflammatory injury

Effect of intermittent hypoxia or hyperoxia on lung development in preterm rat neonates during constant oxygen therapy

Intrauterine Hypoxia and Epigenetic Programming in Lung Development and Disease

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