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Neonatal hyperoxia mouse

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https://www.readbyqxmd.com/read/29079808/hyperoxia-causes-mir-34a-mediated-injury-via-angiopoietin-1-in-neonatal-lungs
#1
Mansoor Syed, Pragnya Das, Aishwarya Pawar, Zubair H Aghai, Anu Kaskinen, Zhen W Zhuang, Namasivayam Ambalavanan, Gloria Pryhuber, Sture Andersson, Vineet Bhandari
Hyperoxia-induced acute lung injury (HALI) is a key contributor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preventive or therapeutic agent is available. Here we show that lung micro-RNA (miR)-34a levels are significantly increased in lungs of neonatal mice exposed to hyperoxia. Deletion or inhibition of miR-34a improves the pulmonary phenotype and BPD-associated pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened by miR-34a overexpression...
October 27, 2017: Nature Communications
https://www.readbyqxmd.com/read/29075011/neonatal-exposure-to-high-oxygen-levels-leads-to-impaired-ischemia-induced-neovascularization-in-adulthood
#2
Raphael Mathieu, Sylvie Dussault, Michel Desjarlais, François Rivard, Wahiba Dhahri, Anik Cloutier, Anne-Monique Nuyt, Alain Rivard
Adverse perinatal conditions can lead to developmental programming of cardiovascular diseases. Prematurely born infants are often exposed to high oxygen levels, which in animal models has been associated with endothelial dysfunction, hypertension, and cardiac remodeling during adulthood. Here we found that adult mice that have been transiently exposed to O2 after birth show defective neovasculariation after hindlimb ischemia, as demonstrated by impaired blood flow recovery, reduced vascular density in ischemic muscles and increased tissue damages...
October 26, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29056548/human-induced-pluripotent-stem-cell-derived-lung-progenitor-and-alveolar-epithelial-cells-attenuate-hyperoxia-induced-lung-injury
#3
Mehdi Shafa, Lavinia Iuliana Ionescu, Arul Vadivel, Jennifer J P Collins, Liqun Xu, Shumei Zhong, Martin Kang, Geneviève de Caen, Manijeh Daneshmand, Jenny Shi, Katherine Z Fu, Andrew Qi, Ying Wang, James Ellis, William L Stanford, Bernard Thébaud
BACKGROUND AIMS: Bronchopulmonary dysplasia (BPD), a chronic lung disease characterized by disrupted lung growth, is the most common complication in extreme premature infants. BPD leads to persistent pulmonary disease later in life. Alveolar epithelial type 2 cells (AEC2s), a subset of which represent distal lung progenitor cells (LPCs), promote normal lung growth and repair. AEC2 depletion may contribute to persistent lung injury in BPD. We hypothesized that induced pluripotent stem cell (iPSC)-derived AECs prevent lung damage in experimental oxygen-induced BPD...
October 20, 2017: Cytotherapy
https://www.readbyqxmd.com/read/29038359/hyperoxia-reduces-insulin-release-and-induces-mitochondrial-dysfunction-with-possible-implications-for-hyperoxic-treatment-of-neonates
#4
Ingrid Hals, Tsuyoshi Ohki, Rinku Singh, Zuheng Ma, Anneli Björklund, Chandima Balasuriya, Hanne Scholz, Valdemar Grill
We previously showed that hyperoxia in vitro negatively affects beta cells of the rat. Here, we tested for possible clinical significance as well as mitochondrial interactions by hyperoxia, using human islets (function and viability), INS-1 832/13 cells (mitochondrial metabolism), and mouse neonates (effects in vivo). Lastly, we assessed relevant parameters in a cohort of individuals born preterm and then exposed to hyperoxia. Human islets and INS-1 832/13 cells were exposed to 24 h of hyperoxia (90-92% oxygen)...
October 2017: Physiological Reports
https://www.readbyqxmd.com/read/29027762/fresh-noncultured-endothelial-progenitor-cells-improve-neonatal-lung-hyperoxia-induced-alveolar-injury
#5
Alexandra B Firsova, A Daniel Bird, Degu Abebe, Judy Ng, Richard Mollard, Timothy J Cole
Treatment of preterm human infants with high oxygen can result in disrupted lung alveolar and vascular development. Local or systemic administration of endothelial progenitor cells (EPCs) is reported to remedy such disruption in animal models. In this study, the effects of both fresh (enriched for KDR) and cultured bone marrow (BM)-derived cell populations with EPC characteristics were examined following hyperoxia in neonatal mouse lungs. Intraperitoneal injection of fresh EPCs into five-day-old mice treated with 90% oxygen resulted in full recovery of hyperoxia-induced alveolar disruption by 56 days of age...
October 13, 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28851267/expression-profiling-of-genes-regulated-by-sphingosine-kinase1-signaling-in-a-murine-model-of-hyperoxia-induced-neonatal-bronchopulmonary-dysplasia
#6
Viswanathan Natarajan, Alison W Ha, Yangbasai Dong, Narsa M Reddy, David L Ebenezer, Prasad Kanteti, Sekhar P Reddy, J Usha Raj, Zhengdeng Lei, Mark Maienschein-Cline, Zarema Arbieva, Anantha Harijith
BACKGROUND: Sphingosine- 1-Phosphate (S1P) is a bioactive lipid and an intracellular as well as an extracellular signaling molecule. S1P ligand specifically binds to five related cell surface G-protein-coupled receptors (S1P1-5). S1P levels are tightly regulated by its synthesis catalyzed by sphingosine kinases (SphKs) 1 & 2 and catabolism by S1P phosphatases, lipid phosphate phosphatases and S1P lyase. We previously reported that knock down of SphK1 (Sphk1 (-/-) ) in a neonatal mouse BPD model conferred significant protection against hyperoxia induced lung injury...
August 29, 2017: BMC Genomics
https://www.readbyqxmd.com/read/28819748/lipoxin-a4-attenuates-bronchopulmonary-dysplasia-via-upregulation-of-let-7c-and-downregulation-of-tgf-%C3%AE-1-signaling-pathway
#7
Xiao-Qing Chen, Sheng-Hua Wu, Yan-Yan Luo, Bing-Jie Li, Shu-Jun Li, Hong-Yan Lu, Rui Jin, Zhong-Yi Sun
Transforming growth factor-β (TGF-β) superfamily members are key regulators for lung development and progress of bronchopulmonary dysplasia (BPD). The mechanisms by which lipoxin A4 (LXA4) attenuates development of BPD have not been clarified. Neonatal murine BPD models were inducted by hyperoxia treatment. Neonatal mice were exposed to room air or 85% O2 hyperoxia with or without treatment with 5S,6R-methyl-LXA4 or anti-TGF-β antibodies. Mouse lung epithelial cells (MLE-12 cells) and mouse embryonic fibroblasts (NIH/3T3 cells) were cultured in room air or 85% O2 followed by treatment of LXA4, anti-TGF-β antibodies, and let-7c mimic/anti-microRNA transfections...
December 2017: Inflammation
https://www.readbyqxmd.com/read/28802561/recombinant-human-elafin-promotes-alveologenesis-in-newborn-mice-exposed-to-chronic-hyperoxia
#8
Wenli Han, Xiaomei Li, Han Zhang, Benli Yu, Chunbao Guo, Chun Deng
BACKGROUND/AIMS: Elastase inhibitors reverse elastin degradation and abnormal alveologenesis and attenuate the lung structural abnormalities induced by mechanical ventilation with O2-rich gas. The potential of these molecules to improve endothelial function and to ameliorate severe bronchopulmonary dysplasia (BPD) during lung development is not yet understood. We sought to determine whether the intratracheal treatment of newborn mice with the elastase inhibitor elafin would prevent hyperoxia-induced lung elastin degradation and the cascade of events that cause abnormal alveologenesis...
August 10, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28798254/oxygen-dependent-changes-in-lung-development-do-not-affect-epithelial-infection-with-influenza-a-virus
#9
William Domm, Min Yee, Ravi S Misra, Robert Gelein, Aitor Nogales, Luis Martinez Sobrido, Michael A O'Reilly
Infants born prematurely often require supplemental oxygen that contributes to aberrant lung development and increased pulmonary morbidity following a respiratory viral infection. We have been using a mouse model to understand how early-life hyperoxia affects the adult lung response to influenza A virus (IAV) infection. Prior studies showed how neonatal hyperoxia (100% oxygen) increased sensitivity of adult mice to infection with influenza A virus (IAV (A/Hong Kong/X31) H3N2) as defined by persistent inflammation, pulmonary fibrosis, and mortality...
August 10, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28583585/effects-of-the-notch-signalling-pathway-on-hyperoxia-induced-immature-brain-damage-in-newborn-mice
#10
Min Du, Yuting Tan, Guangjian Liu, Lan Liu, Fei Cao, Jianxia Liu, Pu Jiang, Ying Xu
Hyperoxia exposure can cause dramatic release of proinflammatory cytokines, leading to neuronal apoptosis and inducing white matter damage in newborn mouse brains. Some studies indicated that the Notch activation was provoked during inflammation and might regulate adaptive and innate immune responses. Moreover, the pathway also regulated oligodendrocyte maturation which was disrupted in neonatal mice after hyperoxia exposure. This study sought to investigate whether the Notch signalling activation contributed to immature brain damage after hyperoxia exposure...
July 13, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28473324/mir-29b-supplementation-decreases-expression-of-matrix-proteins-and-improves-alveolarization-in-mice-exposed-to-maternal-inflammation-and-neonatal-hyperoxia
#11
Shaheen Durrani-Kolarik, Caylie A Pool, Ashley Gray, Kathryn M Heyob, Mary J Cismowski, Gloria Pryhuber, L James Lee, Zhaogang Yang, Trent E Tipple, Lynette K Rogers
Even with advances in the care of preterm infants, chronic lung disease or bronchopulmonary dysplasia (BPD) continues to be a significant pulmonary complication. Among those diagnosed with BPD, a subset of infants develop severe BPD with disproportionate pulmonary morbidities. In addition to decreased alveolarization, these infants develop obstructive and/or restrictive lung function due to increases in or dysregulation of extracellular matrix proteins. Analyses of plasma obtained from preterm infants during the first week of life indicate that circulating miR-29b is suppressed in infants that subsequently develop BPD and that decreased circulating miR-29b is inversely correlated with BPD severity...
August 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28458035/vitamin-a-and-retinoic-acid-combination-attenuates-neonatal-hyperoxia-induced-neurobehavioral-impairment-in-adult-mice
#12
Manimaran Ramani, Thomas van Groen, Inga Kadish, Namasivayam Ambalavanan, Lori L McMahon
Preterm infants exposed to supra-physiological levels of oxygen often have poor executive and memory function associated with reductions in hippocampal volume later in life. We recently showed that adult mice exposed to neonatal hyperoxia have deficits in spatial navigation and increased exploratory behavior associated with hippocampal shrinkage. Retinoids attenuate hyperoxia-induced lung injury in animal models and reduce neonatal chronic lung disease in preterm infants. We hypothesized that retinoid (combination of Vitamin A+Retinoic Acid [VARA]) administration in mice during neonatal hyperoxia would attenuate oxygen-induced cognitive impairment when assessed in adult life...
April 27, 2017: Neurobiology of Learning and Memory
https://www.readbyqxmd.com/read/28438602/hyperoxia-exposure-disrupts-adrenomedullin-signaling-in-newborn-mice-implications-for-lung-development-in-premature-infants
#13
Renuka T Menon, Amrit Kumar Shrestha, Binoy Shivanna
Hyperoxia contributes to the development of bronchopulmonary dysplasia (BPD), a chronic lung disease of human infants that is characterized by disrupted lung angiogenesis. Adrenomedullin (AM) is a multifunctional peptide with angiogenic and vasoprotective properties. AM signals via its cognate receptors, calcitonin receptor-like receptor (Calcrl) and receptor activity-modifying protein 2 (RAMP2). Whether hyperoxia affects the pulmonary AM signaling pathway in neonatal mice and whether AM promotes lung angiogenesis in human infants are unknown...
June 3, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28241859/human-amnion-epithelial-cells-rescue-cell-death-via-immunomodulation-of-microglia-in-a-mouse-model-of-perinatal-brain-injury
#14
Bryan Leaw, Dandan Zhu, Jean Tan, Ruth Muljadi, Mohamed I Saad, Joanne C Mockler, Euan M Wallace, Rebecca Lim, Mary Tolcos
BACKGROUND: Human amnion epithelial cells (hAECs) are clonogenic and have been proposed to reduce inflammatory-induced tissue injury. Perturbation of the immune response is implicated in the pathogenesis of perinatal brain injury; modulating this response could thus be a novel therapy for treating or preventing such injury. The immunomodulatory properties of hAECs have been shown in other animal models, but a detailed investigation of the effects on brain immune cells following injury has not been undertaken...
February 28, 2017: Stem Cell Research & Therapy
https://www.readbyqxmd.com/read/27792858/exposure-to-high-concentration-oxygen-in-the-neonatal-period-induces-abnormal-retinal-vascular-patterning-in-mice
#15
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...
December 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
#16
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...
January 2017: Journal of Pathology
https://www.readbyqxmd.com/read/27532877/nurr1-expression-is-modified-by-inflammation-in-microglia
#17
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
#18
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
#19
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
#20
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
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