scholarly journals Combined effects of maternal inflammation and neonatal hyperoxia on lung fibrosis and RAGE expression in newborn rats

2013 ◽  
Vol 75 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Chien-Ling Su ◽  
Hsiu-Chu Chou ◽  
Liang-Ti Huang ◽  
Tsu-Fu Yeh ◽  
Chung-Ming Chen
Keyword(s):  
Lung Fibrosis ◽  
Combined Effects ◽  
Newborn Rats ◽  
Maternal Inflammation ◽  
Neonatal Hyperoxia ◽  
Rage Expression

Maternal Inflammation and Neonatal Hyperoxia Results in Adult Pulmonary Fibrosis

2010 ◽  
Vol 49 ◽  
pp. S50
Author(s):  
Lynette K Rogers ◽  
Trent E Tipple ◽  
Kathryn M Heyob ◽  
Markus Velten
Keyword(s):  
Pulmonary Fibrosis ◽  
Maternal Inflammation ◽  
Neonatal Hyperoxia

Angiotensin II Type 1 Receptor Antagonist Attenuates Lung Fibrosis in Hyperoxia-Exposed Newborn Rats

2011 ◽  
Vol 340 (1) ◽  
pp. 169-175 ◽  
Author(s):  
Hsiu-Chu Chou ◽  
Yaw-Dong Lang ◽  
Leng-Fang Wang ◽  
Tzu-Ying Wu ◽  
Yu-Fang Hsieh ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Lung Fibrosis ◽  
Newborn Rats

scholarly journals Neonatal Hyperoxia Increases Sensitivity of Adult Mice to Bleomycin-Induced Lung Fibrosis

2013 ◽  
Vol 48 (2) ◽  
pp. 258-266 ◽  
Author(s):  
Min Yee ◽  
Bradley W. Buczynski ◽  
B. Paige Lawrence ◽  
Michael A. O’Reilly
Keyword(s):  
Lung Fibrosis ◽  
Adult Mice ◽  
Neonatal Hyperoxia

scholarly journals Of mice and men: correlations between microRNA-17∼92 cluster expression and promoter methylation in severe bronchopulmonary dysplasia

2016 ◽  
Vol 311 (5) ◽  
pp. L981-L984 ◽  
Author(s):  
Mary E. Robbins ◽  
Duaa Dakhlallah ◽  
Clay B. Marsh ◽  
Lynette K. Rogers ◽  
Trent E. Tipple
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Premature Infants ◽  
Gestational Age ◽  
Murine Model ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
Human Infants ◽  
Qrt Pcr ◽  
Maternal Inflammation ◽  
Neonatal Hyperoxia

We previously demonstrated that decreased miR-17∼92 cluster expression was 1) present in lungs from human infants who died with bronchopulmonary dysplasia (BPD); 2) inversely correlated with DNA methyltransferase (DNMT) expression and promoter methylation; and 3) correlated with a subsequent diagnosis of BPD at 36 wk gestational age. We tested the hypothesis that plasma miR-17 levels would be lowest in infants who ultimately develop severe BPD. Secondly, we utilized our well-characterized murine model of severe BPD that combines perinatal inflammation with postnatal hyperoxia to test the hypothesis that alterations in lung miR-17∼92, DNMT, and promoter methylation in our model would mirror our findings in tissues from premature human infants. Plasma was obtained during the first 5 days of life from premature infants born ≤32 wk gestation. Lung tissues were harvested from mice exposed to maternal inflammation and neonatal hyperoxia for 14 days after birth. miR-17∼92 cluster expression and DNA methyltransferase expression were measured by qRT-PCR, and promoter methylation was assessed by Methyl-Profiler assay. Plasma miR-17 levels are significantly lower in the first week of life in human infants who develop severe BPD compared with mild or moderate BPD. Data from our severe BPD murine model reveal that lung miR-17∼92 cluster expression is significantly attenuated, and levels inversely correlated with DNMT expression and miR-17∼92 cluster promoter methylation. Collectively, our data support a plausible role for epigenetically altered miR-17∼92 cluster in the pathogenesis of severe BPD.

Combined effects of caffeine and alcohol during pregnancy on bones in newborn rats

1996 ◽  
Vol 196 (1) ◽  
pp. 179-185
Author(s):  
T. S. Case ◽  
M. J. Saltzman ◽  
J. Cheuk ◽  
M. Yazdani ◽  
A. Sadeghpour ◽  
...  
Keyword(s):  
Combined Effects ◽  
Newborn Rats

scholarly journals Deficits in lung alveolarization and function after systemic maternal inflammation and neonatal hyperoxia exposure

2010 ◽  
Vol 108 (5) ◽  
pp. 1347-1356 ◽  
Author(s):  
Markus Velten ◽  
Kathryn M. Heyob ◽  
Lynette K. Rogers ◽  
Stephen E. Welty
Keyword(s):  
Pulmonary Function ◽  
Interstitial Fibrosis ◽  
Pulmonary Function Tests ◽  
Combined Treatment ◽  
Lung Mechanics ◽  
Diffuse Fibrosis ◽  
Maternal Inflammation ◽  
Hyperoxia Exposure ◽  
And Function ◽  
Neonatal Hyperoxia

Systemic maternal inflammation contributes to preterm birth and is associated with development of bronchopulmonary dysplasia (BPD). Infants with BPD exhibit decreased alveolarization, diffuse interstitial fibrosis with thickened alveolar septa, and impaired pulmonary function. We tested the hypothesis that systemic prenatal LPS administration to pregnant mice followed by postnatal hyperoxia exposure is associated with prolonged alterations in pulmonary structure and function after return to room air (RA) that are more severe than hyperoxia exposure alone. Timed-pregnant C3H/HeN mice were dosed with LPS (80 μg/kg) or saline on gestation day 16. Newborn pups were exposed to RA or 85% O2 for 14 days and then to RA for an additional 14 days. Data were collected and analyzed on postnatal days 14 and 28. The combination of prenatal LPS and postnatal hyperoxia exposure generated a phenotype with more inflammation (measured as no. of macrophages per high-power field) than either insult alone at day 28. The combined exposures were associated with a diffuse fibrotic response [measured as hydroxyproline content (μg)] but did not induce a more severe developmental arrest than hyperoxia alone. Pulmonary function tests indicated that hyperoxia, independent of maternal exposure, induced compliance decreases on day 14 that did not persist after RA recovery. Either treatment alone or combined induced an increase in resistance on day 14, but the increase persisted on day 28 only in pups receiving the combined treatment. In conclusion, the combination of systemic maternal inflammation and neonatal hyperoxia induced a prolonged phenotype of arrested alveolarization, diffuse fibrosis, and impaired lung mechanics that mimics human BPD. This new model should be useful in designing studies of specific mechanisms and interventions that could ultimately be utilized to define therapies to prevent BPD in premature infants.

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