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Neonatal hyperoxia mouse

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https://www.readbyqxmd.com/read/27792858/exposure-to-high-concentration-oxygen-in-the-neonatal-period-induces-abnormal-retinal-vascular-patterning-in-mice
#1
Akane Morita, Hiroko Ushikubo, Asami Mori, Kenji Sakamoto, Tsutomu Nakahara
The interruption of vascular development could cause structural and functional abnormalities in tissues. We have previously reported that short-term treatment of newborn mice with vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors induces abnormal retinal vascular growth and patterns. An exposure of neonatal mice to high-concentration oxygen disturbs normal retinal vascular development. The present study aimed to determine (1) whether vascular abnormalities are observed in the retina of newborn mice exposed to high concentrations of oxygen, and (2) how astrocyte network formation is affected following the exposure to hyperoxia...
October 28, 2016: Birth Defects Research. Part B, Developmental and Reproductive Toxicology
https://www.readbyqxmd.com/read/27770432/fgf10-deficiency-is-causative-for-lethality-in-a-mouse-model-of-bronchopulmonary-dysplasia
#2
Cho-Ming Chao, Faady Yahya, Alena Moiseenko, Caterina Tiozzo, Amit Shrestha, Negah Ahmadvand, Elie El Agha, Jennifer Quantius, Salma Dilai, Vahid Kheirollahi, Matthew Jones, Jochen Wilhem, Gianni Carraro, Harald Ehrhardt, Klaus-Peter Zimmer, Guillermo Barreto, Katrin Ahlbrecht, Rory E Morty, Susanne Herold, Rosanna G Abellar, Werner Seeger, Ralph Schermuly, Jin-San Zhang, Parviz Minoo, Saverio Bellusci
Inflammation-induced FGF10 protein deficiency is associated with bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurely born infants characterized by arrested alveolar development. So far, experimental evidence for a direct role of FGF10 in lung disease is lacking. Using the hyperoxia-induced neonatal lung injury as a mouse model of BPD, the impact of Fgf10 deficiency in Fgf10(+/-) versus Fgf10(+/+) pups was investigated. In normoxia, no lethality of Fgf10(+/+) or Fgf10(+/-) pups was observed...
October 22, 2016: Journal of Pathology
https://www.readbyqxmd.com/read/27532877/nurr1-expression-is-modified-by-inflammation-in-microglia
#3
Scott W Lallier, Amanda E Graf, Gavisha R Waidyarante, Lynette K Rogers
Advances in neonatal care have allowed premature infants to survive at earlier gestational ages, but they are often afflicted with neurological delays or deficits. Maternal inflammation has been identified as a major risk factor for premature birth and once born, infants often require supplemental oxygen for survival. Nurr1 (NR4A2) is an orphan nuclear receptor with no known binding site and is essential for the growth of midbrain dopamine neurons. Others have reported that Nurr1 can act as an anti-inflammatory transcription factor in microglia and astrocytes and respond lipopolysaccharide (LPS)...
October 19, 2016: Neuroreport
https://www.readbyqxmd.com/read/27484068/s-nitrosoglutathione-attenuates-airway-hyperresponsiveness-in-murine-bronchopulmonary-dysplasia
#4
Thomas M Raffay, Andrew M Dylag, Juliann M Di Fiore, Laura A Smith, Helly J Einisman, Yuejin Li, Mitchell M Lakner, Ahmad M Khalil, Peter M MacFarlane, Richard J Martin, Benjamin Gaston
Bronchopulmonary dysplasia (BPD) is characterized by lifelong obstructive lung disease and profound, refractory bronchospasm. It is observed among survivors of premature birth who have been treated with prolonged supplemental oxygen. Therapeutic options are limited. Using a neonatal mouse model of BPD, we show that hyperoxia increases activity and expression of a mediator of endogenous bronchoconstriction, S-nitrosoglutathione (GSNO) reductase. MicroRNA-342-3p, predicted in silico and shown in this study in vitro to suppress expression of GSNO reductase, was decreased in hyperoxia-exposed pups...
October 2016: Molecular Pharmacology
https://www.readbyqxmd.com/read/27343195/mir-196a-regulates-heme-oxygenase-1-by-silencing-bach1-in-the-neonatal-mouse-lung
#5
Hayato Go, Ping La, Fumihiko Namba, Masato Ito, Guang Yang, Andrey Brydun, Kazuhiko Igarashi, Phyllis A Dennery
In the lung, heme oxygenase-1 (HO-1) is developmentally regulated, with its highest expression in the first days of life. In addition, neonatal mice have limited HO-1 induction in hyperoxia compared with adults. However, few reports have addressed the functional effect of microRNAs (miRNAs) in the regulation of HO-1 in vivo. The aims of the present study were to characterize changes in lung miRNA expression during postnatal development and in response to hyperoxic exposure, and to identify miRNAs that target lung HO-1 gene expression...
August 1, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/27279073/protective-effects-of-bmscs-in-combination-with-erythropoietin-in-bronchopulmonary-dysplasia-induced-lung-injury
#6
Zhao-Hua Zhang, Yan-Yan Pan, Rui-Sheng Jing, Yun Luan, Luan Zhang, Chao Sun, Feng Kong, Kai-Lin Li, Yi-Biao Wang
Bronchopulmonary dysplasia (BPD) is the most common type of chronic lung disease in infancy, for which no effective therapy is currently available. The aim of the present study was to investigate the effect of treatment with bone marrow mesenchymal stem cells (BMSCs) in combination with recombinant human erythropoietin (rHuEPO) on BPD‑induced mouse lung injury, and discuss the underlying mechanism. The BPD model was established by the exposure of neonatal mice to continuous high oxygen exposure for 14 days, following which 1x106 BMSCs and 5,000 U/kg rHuEPO were injected into the mice 1 h prior to and 7 days following exposure to hyperoxia...
August 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27137150/differential-expression-of-long-non-coding-rnas-in-hyperoxia-induced-bronchopulmonary-dysplasia
#7
Tian-Ping Bao, Rong Wu, Huai-Ping Cheng, Xian-Wei Cui, Zhao-Fang Tian
Bronchopulmonary dysplasia (BPD) is a common complication of premature birth that seriously affects the survival rate and quality of life among preterm neonates. Long non-coding RNAs (lncRNAs) have been implicated in many human diseases. However, the role of lncRNAs in the pathogenesis of BPD remains poorly understood. Here, we exposed neonatal C57BL/6J mice to 95% concentrations of ambient oxygen and established a mouse lung injury model that mimicked human BPD. Next, we compared lncRNA and messenger RNA (mRNA) expression profiles between BPD and normal lung tissues using a high-throughput mouse lncRNA + mRNA array system...
July 2016: Cell Biochemistry and Function
https://www.readbyqxmd.com/read/27116319/neonatal-hyperoxia-increases-airway-reactivity-and-inflammation-in-adult-mice
#8
Vasantha H S Kumar, Satyan Lakshminrusimha, Sergei Kishkurno, Babu S Paturi, Sylvia F Gugino, Lori Nielsen, Huamei Wang, Rita M Ryan
BACKGROUND: Supplemental O2 to treat bronchopulmonary dysplasia (BPD) in premature infants, is a major risk factor producing alteration in lung function, airway reactivity, and predisposition to respiratory infections. This study explores inflammatory and airway responses following neonatal hyperoxia in adult mice. METHODS: Newborn mouse litters were randomized to 85% O2 or room air (RA) on P3 for 12 days; mice were sacrificed either on P15 or at 15 weeks following recovery in RA...
April 26, 2016: Pediatric Pulmonology
https://www.readbyqxmd.com/read/27070483/sex-related-differences-in-long-term-pulmonary-outcomes-of-neonatal-hyperoxia-in-mice
#9
Fumihiko Namba, Ryo Ogawa, Masato Ito, Takaaki Watanabe, Phyllis A Dennery, Masanori Tamura
AIM: Premature infants are often exposed to hyperoxia to maintain adequate oxygenation, which may lead to the development of bronchopulmonary dysplasia (BPD). Sex-specific differences exist in the development and severity of BPD. Only a few studies have examined the mechanisms underlying these sex-related differences. The aim of the present study is to examine the sex-related long-term effects of neonatal hyperoxia on the lungs of adult mice. MATERIALS AND METHODS: Newborn mice were exposed to 95% oxygen (hyperoxia) for 96 hours and were allowed to recover in room air to adulthood (8 weeks of age)...
2016: Experimental Lung Research
https://www.readbyqxmd.com/read/26938952/hyperoxia-induces-intracellular-acidification-in-neonatal-mouse-lung-fibroblasts-real-time-investigation-using-plasmonically-enhanced-raman-spectroscopy
#10
Sajanlal R Panikkanvalappil, Masheika James, Steven M Hira, James Mobley, Tamas Jilling, Namasivayam Ambalavanan, Mostafa A El-Sayed
It is important to understand the molecular mechanisms underlying oxygen toxicity, which contributes to multiple human disorders. The archetype model of oxygen toxicity is neonatal lung injury induced by hyperoxia exposure. Here, we utilized plasmonically enhanced Raman spectroscopy (PERS) in combination with fluorescence and proteomic analysis to provide comprehensive information on hyperoxia-induced biomolecular modifications in neonatal mouse lung fibroblasts (nMLFs). During this study, we made the novel observation that hyperoxia induces intracellular acidification in nMLF, which we probed in real-time using label-free PERS...
March 23, 2016: Journal of the American Chemical Society
https://www.readbyqxmd.com/read/26878215/initial-suppression-of-transforming-growth-factor-%C3%AE-signaling-and-loss-of-tgfbi-causes-early-alveolar-structural-defects-resulting-in-bronchopulmonary-dysplasia
#11
Shawn K Ahlfeld, Jian Wang, Yong Gao, Paige Snider, Simon J Conway
Septation of the gas-exchange saccules of the morphologically immature mouse lung requires regulated timing, spatial direction, and dosage of transforming growth factor (TGF)-β signaling. We found that neonatal hyperoxia acutely initially diminished saccular TGF-β signaling coincident with alveolar simplification. However, sustained hyperoxia resulted in a biphasic response and subsequent up-regulation of TGF-β signaling, ultimately resulting in bronchopulmonary dysplasia. Significantly, we found that the TGF-β-induced matricellular protein (TGFBI) was similarly biphasically altered in response to hyperoxia...
April 2016: American Journal of Pathology
https://www.readbyqxmd.com/read/26756781/dose-dependent-effects-of-glucocorticoids-on-pulmonary-vascular-development-in-a-murine-model-of-hyperoxic-lung-injury
#12
Marta Perez, Kamila Wisniewska, Keng Jin Lee, Herminio J Cardona, Joann M Taylor, Kathryn N Farrow
BACKGROUND: Exposure of neonatal mice to hyperoxia results in pulmonary vascular remodeling and aberrant phosphodiesterase type 5 (PDE5) signaling. Although glucocorticoids are frequently utilized in the NICU, little is known about their effects on the developing pulmonary vasculature and on PDE5. We sought to determine the effects of hydrocortisone (HC) on pulmonary vascular development and on PDE5 in a neonatal mouse model of hyperoxic lung injury. METHODS: C57BL/6 mice were placed in 21% O2 or 75% O2 within 24 h of birth and received HC (1, 5, or 10 mg/kg subcutaneously every other day) or vehicle...
May 2016: Pediatric Research
https://www.readbyqxmd.com/read/26688580/neuroprotective-effect-of-myo-nog-cells-in-the-stressed-retina
#13
Arturo Bravo-Nuevo, Alice A Brandli, Jacquelyn Gerhart, Jennifer Nichols, Meghan Pitts, Christopher K Sutera, Sarah Assali, Victoria Scheinfeld, George C Prendergast, Jonathan Stone, Mindy George-Weinstein
Myo/Nog cells are essential for eye development in the chick embryo and respond to injury in adult tissues. These cells express mRNA for the skeletal muscle specific transcription factor MyoD, the bone morphogenetic protein (BMP) inhibitor Noggin and the cell surface protein recognized by the G8 monoclonal antibody (mAb). In this study, we determined that Myo/Nog cells are present in low numbers in the retina of the mouse eye. G8-positive Myo/Nog cells were distinguished from neuronal, Müller and microglial cells that were identified with antibodies to calretinin, Chx10, glial fibrillary acidic protein and ionized calcium binding adaptor molecule 1, respectively...
May 2016: Experimental Eye Research
https://www.readbyqxmd.com/read/26593641/the-in-vivo-respiratory-phenotype-of-the-adenosine-a1-receptor-knockout-mouse
#14
Dirk Heitzmann, Philipp Buehler, Frank Schweda, Michael Georgieff, Richard Warth, Joerg Thomas
The nucleoside adenosine has been implicated in the regulation of respiration, especially during hypoxia in the newborn. In this study the role of adenosine A1 receptors for the control of respiration was investigated in vivo. To this end, respiration of unrestrained adult and neonatal adenosine A1 receptor knockout mice (A1R(-/-)) was measured in a plethysmographic device. Under control conditions (21% O2) and mild hypoxia (12-15% O2) no difference of respiratory parameters was observed between adult wildtype (A1R(+/+)) and A1R(-/-) mice...
February 1, 2016: Respiratory Physiology & Neurobiology
https://www.readbyqxmd.com/read/26539665/effects-of-antenatal-lipopolysaccharide-and-postnatal-hyperoxia-on-airway-reactivity-and-remodeling-in-a-neonatal-mouse-model
#15
Arij Faksh, Rodney D Britt, Elizabeth R Vogel, Ine Kuipers, Michael A Thompson, Gary C Sieck, Christina M Pabelick, Richard J Martin, Y S Prakash
BACKGROUND: Antenatal inflammation and preterm birth are associated with the development of airway diseases such as wheezing and asthma. Utilizing a newborn mouse model, we assessed the effects of maternal inflammation and postnatal hyperoxia on the neonatal airway. METHODS: Pregnant C57/Bl6 dams were injected with lipopolysaccharide (LPS) or saline on embryonic day 16. Offspring were placed in room air or hyperoxia (50% O2) for 7 d and then returned to normoxia...
March 2016: Pediatric Research
https://www.readbyqxmd.com/read/26509921/effect-of-hyperoxia-on-retinoid-metabolism-and-retinoid-receptor-expression-in-the-lungs-of-newborn-mice
#16
Hsing-Jin Chen, Bor-Luen Chiang
BACKGROUND: Preterm newborns that receive oxygen therapy often develop bronchopulmonary dysplasia (BPD), which is abnormal lung development characterized by impaired alveologenesis. Oxygen-mediated injury is thought to disrupt normal lung growth and development. However, the mechanism of hyperoxia-induced BPD has not been extensively investigated. We established a neonatal mouse model to investigate the effects of normobaric hyperoxia on retinoid metabolism and retinoid receptor expression...
2015: PloS One
https://www.readbyqxmd.com/read/26394387/the-effect-of-continuous-positive-airway-pressure-in-a-mouse-model-of-hyperoxic-neonatal-lung-injury
#17
Brent Reyburn, Juliann M Di Fiore, Thomas Raffay, Richard J Martin, Y S Prakash, Anjum Jafri, Peter M MacFarlane
BACKGROUND: Continuous positive airway pressure (CPAP) and supplemental oxygen have become the mainstay of neonatal respiratory support in preterm infants. Although oxygen therapy is associated with respiratory morbidities including bronchopulmonary dysplasia (BPD), the long-term effects of CPAP on lung function are largely unknown. We used a hyperoxia-induced mouse model of BPD to explore the effects of daily CPAP in the first week of life on later respiratory system mechanics. OBJECTIVE: We wanted to test the hypothesis that daily CPAP in a newborn-mouse model of BPD improves longer-term respiratory mechanics...
2016: Neonatology
https://www.readbyqxmd.com/read/26361877/can-maternal-dha-supplementation-offer-long-term-protection-against-neonatal-hyperoxic-lung-injury
#18
REVIEW
Krithika Lingappan, Bhagavatula Moorthy
The effect of adverse perinatal environment (like maternal infection) has long-standing effects on many organ systems, including the respiratory system. Use of maternal nutritional supplements is an exciting therapeutic option that could be used to protect the developing fetus. In a recent issue of the journal, Ali and associates (Ali M, Heyob KM, Velten M, Tipple TE, Rogers LK. Am J Physiol Lung Cell Mol Physiol 309: L441-L448, 2015) specifically look at maternal docosahexaenoic acid (DHA) supplementation and its effect on chronic apoptosis in the lung in a mouse model of perinatal inflammation and postnatal hyperoxia...
December 15, 2015: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/26192732/cd11b-mononuclear-cells-mitigate-hyperoxia-induced-lung-injury-in-neonatal-mice
#19
Laurie C Eldredge, Piper M Treuting, Anne M Manicone, Steven F Ziegler, William C Parks, John K McGuire
Bronchopulmonary dysplasia (BPD) is a common consequence of life-saving interventions for infants born with immature lungs. Resident tissue myeloid cells regulate lung pathology, but their role in BPD is poorly understood. To determine the role of lung interstitial myeloid cells in neonatal responses to lung injury, we exposed newborn mice to hyperoxia, a neonatal mouse lung injury model with features of human BPD. In newborn mice raised in normoxia, we identified a CD45(+) F4/80(+) CD11b(+), Ly6G(lo-int) CD71(+) population of cells in lungs of neonatal mice present in significantly greater percentages than in adult mice...
February 2016: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/26122393/autophagy-regulates-hyperoxia-induced-intracellular-accumulation-of-surfactant-protein-c-in-alveolar-type-ii-cells
#20
Liang Zhang, Shuang Zhao, Li-Jie Yuan, Hong-Min Wu, Hong Jiang, Shi-Meng Zhao, Gang Luo, Xin-Dong Xue
Surfactant protein C (SP-C) deficiency is a risk factor for hyperoxia-induced bronchopulmonary dysplasia in newborn infants. However, the role of SP-C deficiency in the process is unclear. Here, using neonatal rat BPD model and MLE-12, mouse alveolar epithelial type II cell, we examined the changes of SP-C levels during hyperoxia. Immunohistochemistry, immunofluorescence, and ELISA analysis showed SP-C accumulation in alveolar epithelial type II cells. Electron microscopy further demonstrated the accumulation of lamellar bodies and the co-localization of lamellar bodies with autophagosomes in the cytoplasm of alveolar epithelial type II cells...
October 2015: Molecular and Cellular Biochemistry
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