| Defective pulmonary innervation and autonomic imbalance in congenital diaphragmatic hernia. | |
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MedLine Citation:
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PMID: 22114150 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Congenital diaphragmatic hernia (CDH) is associated with significant mortality due to lung hypoplasia and pulmonary hypertension. The role of embryonic pulmonary innervation in normal lung development and lung maldevelopment in CDH has not been defined. We hypothesize that developmental defects of intrapulmonary innervation, in particular autonomic innervation, occur in CDH. This abnormal embryonic pulmonary innervation may contribute to lung developmental defects and postnatal physiological derangement in CDH. To define patterns of pulmonary innervation in CDH, human CDH and control lung autopsy specimens were stained with the pan-neural marker S-100. To further characterize patterns of overall and autonomic pulmonary innervation during lung development in CDH, the murine nitrofen model of CDH was utilized. Immunostaining for protein gene product 9.5 (a pan-neuronal marker), tyrosine hydroxylase (a sympathetic marker), vesicular acetylcholine transporter (a parasympathetic marker), or VIP (a parasympathetic marker) was performed on lung whole mounts and analyzed via confocal microscopy and three-dimensional reconstruction. Peribronchial and perivascular neuronal staining pattern is less complex in human CDH than control lung. In mice, protein gene product 9.5 staining reveals less complex neuronal branching and decreased neural tissue in nitrofen-treated lungs from embryonic day 12.5 to 16.5 compared with controls. Furthermore, nitrofen-treated embryonic lungs exhibited altered autonomic innervation, with a relative increase in sympathetic nerve staining and a decrease in parasympathetic nerve staining compared with controls. These results suggest a primary defect in pulmonary neural developmental in CDH, resulting in less complex neural innervation and autonomic imbalance. Defective embryonic pulmonary innervation may contribute to lung developmental defects and postnatal physiological derangement in CDH. |
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Authors:
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Nikesh R Lath; Csaba Galambos; Alejandro Best Rocha; Marcus Malek; George K Gittes; Douglas A Potoka |
Publication Detail:
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Type: Journal Article Date: 2011-11-23 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 302 ISSN: 1522-1504 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-02-13 Completed Date: 2012-03-27 Revised Date: 2012-08-30 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L390-8 Citation Subset: IM |
Affiliation:
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Department of Surgery, University of Pittsburgh, PA, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biological Markers / metabolism Case-Control Studies Female Hernia, Diaphragmatic / chemically induced, congenital*, pathology Humans Infant Infant, Newborn Lung / embryology, innervation*, pathology Mice Parasympathetic Nervous System / embryology, metabolism, pathology* Phenyl Ethers Pregnancy S100 Proteins / metabolism Sympathetic Nervous System / embryology, metabolism, pathology* Vasoactive Intestinal Peptide / metabolism Vesicular Acetylcholine Transport Proteins / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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K08 HD061599/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Phenyl Ethers; 0/S100 Proteins; 0/Slc18a3 protein, mouse; 0/Vesicular Acetylcholine Transport Proteins; 1836-75-5/nitrofen; 37221-79-7/Vasoactive Intestinal Peptide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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