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      Rosiglitazone, a Peroxisome Proliferator-Activated Receptor-γ Agonist, Restores Alveolar and Pulmonary Vascular Development in a Rat Model of Bronchopulmonary Dysplasia

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          Abstract

          Purpose

          We tested whether rosiglitazone (RGZ), a peroxisome proliferator-activated receptor-γ agonist, can restore alveolar development and vascular growth in a rat model of bronchopulmonary dysplasia (BPD).

          Materials and Methods

          A rat model of BPD was induced through intra-amniotic delivery of lipopolysaccharide (LPS) and postnatal hyperoxia (80% for 7 days). RGZ (3 mg/kg/d, i.p.) or vehicle was given daily to rat pups for 14 days. This model included four experimental groups: No BPD+vehicle (V), No BPD+RGZ, BPD+V, and BPD+RGZ. On D14, alveolarization, lung vascular density, and right ventricular hypertrophy (RVH) were evaluated.

          Results

          Morphometric analysis revealed that the BPD+RGZ group had significantly smaller and more complex airspaces and larger alveolar surface area than the BPD+V group. The BPD+RGZ group had significantly greater pulmonary vascular density than the BPD+V group. Western blot analysis revealed that significantly decreased levels of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 by the combined exposure to intra-amniotic LPS and postnatal hyperoxia were restored by the RGZ treatment. RVH was significantly lesser in the BPD+RGZ group than in the BPD+V group.

          Conclusion

          These results suggest that RGZ can restore alveolar and pulmonary vascular development and lessen pulmonary hypertension in a rat model of BPD.

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          Bronchopulmonary dysplasia: where have all the vessels gone? Roles of angiogenic growth factors in chronic lung disease.

          Bernard Thébaud, Steven H. Abman (2007)
          Bronchopulmonary dysplasia and emphysema are significant global health problems at the extreme stages of life. Both are characterized by arrested alveolar development or loss of alveoli, respectively. Both lack effective treatment strategies. Knowledge about the genetic control of branching morphogenesis in mammals derives from investigations of the respiratory system in Drosophila, but mechanisms that regulate alveolar development remain poorly understood. Even less is known about regulation of the growth and development of the pulmonary vasculature. Understanding how alveoli and the underlying capillary network develop, and how these mechanisms are disrupted in disease states, are critical for developing effective therapies for lung diseases characterized by impaired alveolar structure. Recent observations have challenged old notions that the development of the blood vessels in the lung passively follows that of the airways. Rather, increasing evidence suggests that lung blood vessels actively promote alveolar growth during development and contribute to the maintenance of alveolar structures throughout postnatal life. Our working hypothesis is that disruption of angiogenesis impairs alveolarization, and that preservation of vascular growth and endothelial survival promotes growth and sustains the architecture of the distal airspace. Furthermore, the explosion of interest in stem cell biology suggests potential roles for endothelial progenitor cells in the pathogenesis or treatment of lung vascular disease. In this Pulmonary Perspective, we review recent data on the importance of the lung circulation, specifically examining the relationship between dysmorphic vascular growth and impaired alveolarization, and speculate on how these new insights may lead to novel therapeutic strategies for bronchopulmonary dysplasia.
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            Chorioamnionitis as a risk factor for bronchopulmonary dysplasia: a systematic review and meta-analysis.

            Lisa Hartling, Yuanyuan Liang, Thierry Lacaze-Masmonteil (2011)
            To conduct a systematic review of the association between chorioamnionitis (CA) and bronchopulmonary dysplasia (BPD) in preterm infants. The authors searched Medline, Embase, CINAHL, Science Citation Index and PubMed, reviewed reference lists and contacted the primary authors of relevant studies. Studies were included if they had a comparison group, examined preterm or low birthweight infants, and provided primary data. Two reviewers independently screened the search results, applied inclusion criteria and assessed methodological quality. One reviewer extracted data and a second reviewer checked data extraction. Studies were combined with an OR using a random effects model. Meta-regression was used to explore potential confounders. 3587 studies were identified; 59 studies (15 295 patients) were included. The pooled unadjusted OR showed that CA was significantly associated with BPD (OR 1.89, 95% CI 1.56 to 2.3). Heterogeneity was substantial (I(2)=66.2%) and may be partially explained by the type of CA. Infants exposed to CA were significantly younger and lighter at birth. The pooled adjusted OR was 1.58 (95% CI 1.11 to 2.24); heterogeneity was substantial (I(2)=65.1%) which may be due to different variables being controlled in each study. There was strong evidence of publication bias which suggests potential overestimation of the measure of association between CA and BPD. Unadjusted and adjusted analyses showed that CA was significantly associated with BPD; however, the adjusted results were more conservative in the magnitude of association. The authors found strong evidence of publication bias. Despite a large body of evidence, CA cannot be definitively considered a risk factor for BPD.
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              Lung vascular development: implications for the pathogenesis of bronchopulmonary dysplasia.

              Kurt Stenmark, Steven H. Abman (2004)
              Past studies have primarily focused on how altered lung vascular growth and development contribute to pulmonary hypertension. Recently, basic studies of vascular growth have led to novel insights into mechanisms underlying development of the normal pulmonary circulation and the essential relationship of vascular growth to lung alveolar development. These observations have led to new concepts underlying the pathobiology of developmental lung disease, especially the inhibition of lung growth that characterizes bronchopulmonary dysplasia (BPD). We speculate that understanding basic mechanisms that regulate and determine vascular growth will lead to new clinical strategies to improve the long-term outcome of premature babies with BPD.
              Article 0 comments Cited 73 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Yonsei Med J
                Journal ID (iso-abbrev): Yonsei Med. J
                Journal ID (publisher-id): YMJ
                Title: Yonsei Medical Journal
                Publisher: Yonsei University College of Medicine
                ISSN (Print): 0513-5796
                ISSN (Electronic): 1976-2437
                Publication date (Print): 01 January 2014
                Publication date (Electronic): 29 November 2013
                Volume: 55
                Issue: 1
                Pages: 99-106
                Affiliations
                [1 ]Department of Pediatrics, Hanyang University Seoul Hospital, Seoul, Korea.
                [2 ]Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, Korea.
                [3 ]Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, Korea.
                [4 ]Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea.
                Author notes
                Corresponding author: Dr. Chang Won Choi, Department of Pediatrics, Seoul National University Bundang Hospital, 82 Gumi-ro 173beon-gil, Bundang-gu, Seongnam 463-707, Korea. Tel: 82-31-787-7286, Fax: 82-31-787-4054, choicw@ 123456snu.ac.kr
                Article
                DOI: 10.3349/ymj.2014.55.1.99
                PMC ID: 3874901
                PubMed ID: 24339293
                SO-VID: 661551e8-45c8-41ed-ba5b-3ed2d21bc68b
                Copyright © © Copyright: Yonsei University College of Medicine 2014
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 April 2013
                Date revision received : 18 June 2013
                Date accepted : 18 June 2013
                Funding
                Funded by: National Research Foundation of Korea
                Award ID: 2010-0021644
                Funded by: Seoul National University Bundang Hospital
                Award ID: 02-2012-006
                Categories
                Subject: Original Article
                Subject: Pulmonology & Critical Care Medicine

                ScienceOpen disciplines: Medicine
                Keywords: bronchopulmonary dysplasia,alveolarization,peroxisome proliferator-activated receptor-γ,rosiglitazone
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: bronchopulmonary dysplasia, alveolarization, peroxisome proliferator-activated receptor-γ, rosiglitazone

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