Epithelial‐mesenchymal transitions in bronchopulmonary dysplasia of newborn rats. Issue 11 (11th April 2014)
- Record Type:
- Journal Article
- Title:
- Epithelial‐mesenchymal transitions in bronchopulmonary dysplasia of newborn rats. Issue 11 (11th April 2014)
- Main Title:
- Epithelial‐mesenchymal transitions in bronchopulmonary dysplasia of newborn rats
- Authors:
- Yang, Haiping
Fu, Jianhua
Xue, Xindong
Yao, Li
Qiao, Lin
Hou, Ana
Jin, Linlin
Xing, Yujiao - Abstract:
- <abstract abstract-type="main" xml:lang="en"> <title>Summary</title> <sec id="ppul22969-sec-0001" sec-type="section"> <title>Background</title> <p>Bronchopulmonary dysplasia (BPD) is a major threat to the health of premature infants yet its pathogenesis is not fully understood. Epithelial‐mesenchymal transition (EMT) of lung epithelial cells may lead to BPD.</p> </sec> <sec id="ppul22969-sec-0002" sec-type="section"> <title>Objective</title> <p>To investigate the potential occurrence of EMT in a newborn rat model of BPD.</p> </sec> <sec id="ppul22969-sec-0003" sec-type="section"> <title>Methods</title> <p>Newborn rats were exposed to a hyperoxic environment within 12 hr of birth. Lung tissue and isolated alveolar epithelial type II cells (AT2 cells) were collected on Days 1, 3, 7, 14, and 21 after hyperoxic exposure. Pathological changes in lung tissue, alveolar development, ultrastructural changes in AT2 cells, co‐expression of surfactant associated surfactant protein C (SPC), and α‐smooth muscle actin (α‐SMA) were investigated. The relative expression of SPC, α‐SMA, E‐cadherin, and N‐cadherin were investigated in lung tissue and isolated AT2 cells.</p> </sec> <sec id="ppul22969-sec-0004" sec-type="section"> <title>Results</title> <p>In lung tissue, alveolar development was attenuated from Day 7 onwards in the BPD model group; co‐expression of SPC and α‐SMA and ultrastructural changes typical of EMT were observed in AT2 cells from rats in the BPD group. SPC and α‐SMA<abstract abstract-type="main" xml:lang="en"> <title>Summary</title> <sec id="ppul22969-sec-0001" sec-type="section"> <title>Background</title> <p>Bronchopulmonary dysplasia (BPD) is a major threat to the health of premature infants yet its pathogenesis is not fully understood. Epithelial‐mesenchymal transition (EMT) of lung epithelial cells may lead to BPD.</p> </sec> <sec id="ppul22969-sec-0002" sec-type="section"> <title>Objective</title> <p>To investigate the potential occurrence of EMT in a newborn rat model of BPD.</p> </sec> <sec id="ppul22969-sec-0003" sec-type="section"> <title>Methods</title> <p>Newborn rats were exposed to a hyperoxic environment within 12 hr of birth. Lung tissue and isolated alveolar epithelial type II cells (AT2 cells) were collected on Days 1, 3, 7, 14, and 21 after hyperoxic exposure. Pathological changes in lung tissue, alveolar development, ultrastructural changes in AT2 cells, co‐expression of surfactant associated surfactant protein C (SPC), and α‐smooth muscle actin (α‐SMA) were investigated. The relative expression of SPC, α‐SMA, E‐cadherin, and N‐cadherin were investigated in lung tissue and isolated AT2 cells.</p> </sec> <sec id="ppul22969-sec-0004" sec-type="section"> <title>Results</title> <p>In lung tissue, alveolar development was attenuated from Day 7 onwards in the BPD model group; co‐expression of SPC and α‐SMA and ultrastructural changes typical of EMT were observed in AT2 cells from rats in the BPD group. SPC and α‐SMA expression levels were higher in tissue samples from the BPD group than in control samples. Beginning on Day 7, evidence of a switch from E‐cadherin to N‐cadherin expression was observed in BPD lung tissue sample and in isolated AT2 cells.</p> </sec> <sec id="ppul22969-sec-0005" sec-type="section"> <title>Conclusion</title> <p>EMT of AT2 cells occurred in the hyperoxia‐induced newborn rat BPD model and resulted in attenuated alveolar development as a portion of the myofibroblasts accumulated in the lung originated from AT2 cells via EMT. <bold>Pediatr Pulmonol. 2014; 49:1112–1123.</bold> © 2014 Wiley Periodicals, Inc.</p> </sec> </abstract> … (more)
- Is Part Of:
- Pediatric pulmonology. Volume 49:Issue 11(2014:Nov.)
- Journal:
- Pediatric pulmonology
- Issue:
- Volume 49:Issue 11(2014:Nov.)
- Issue Display:
- Volume 49, Issue 11 (2014)
- Year:
- 2014
- Volume:
- 49
- Issue:
- 11
- Issue Sort Value:
- 2014-0049-0011-0000
- Page Start:
- 1112
- Page End:
- 1123
- Publication Date:
- 2014-04-11
- Subjects:
- Pediatric respiratory diseases -- Periodicals
Pediatrics -- Periodicals
618.922 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1099-0496 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/ppul.22969 ↗
- Languages:
- English
- ISSNs:
- 8755-6863
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 6417.605800
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3247.xml