| Neonatal lung and airway injury: a role for neurotrophins. | |
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MedLine Citation:
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PMID: 16813975 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Maintenance of patency in distal airways is essential for gas exchange in neonatal life, and its disruption may have long-lasting effects on respiratory function. However, neural mechanisms that regulate caliber of intrapulmonary airways during early postnatal life, and their disruption by hyperoxic exposure, have not been well characterized. We have previously shown that cholinergically mediated airway contractile responses in rat pups are upregulated after hyperoxic exposure, and that increased expression of neuropeptides, such as substance P, may be contributory. More recently, we have documented impairment of neurally mediated airway relaxation in response to hyperoxic stress associated with loss of nitric oxide and prostaglandin-induced airway relaxation as well as inhibition of long chain myosin phosphatase. Our most recent data demonstrate significantly enhanced expression of the neurotrophin, brain-derived neurotrophic factor (BDNF) and its high affinity specific tyrosine kinase B (TrkB) receptor in hyperoxia-exposed airway smooth muscle. The existence of a BDNF-TrkB receptor autocrine and paracrine loops in the airways provides a basis for understanding local regulatory mechanisms of airway homeostasis. A mechanistic role for BDNF-TrkB signaling in hyperoxia-induced airway hyperreactivity in early postnatal life could serve to modulate both afferent and efferent neural pathways that result in enhanced contractile responses of immature airways exposed to hyperoxic stress. Greater insight into these neural pathways may lead to future preventive strategies for preterm infants surviving neonatal intensive care and developing chronic lung disease. |
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Authors:
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Qin Yao; Syed I Zaidi; Musa A Haxhiu; Richard J Martin |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: Seminars in perinatology Volume: 30 ISSN: 0146-0005 ISO Abbreviation: Semin. Perinatol. Publication Date: 2006 Jun |
Date Detail:
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Created Date: 2006-07-03 Completed Date: 2006-12-01 Revised Date: 2007-12-03 |
Medline Journal Info:
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Nlm Unique ID: 7801132 Medline TA: Semin Perinatol Country: United States |
Other Details:
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Languages: eng Pagination: 156-62 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, Case Western Reserve University School of Medicine, Case Western Reserve University School of Medicine, Rainbow Babies and Children's Hospital, 11100 Euclid Avenue, Cleveland, OH 44106, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Animals, Newborn Autocrine Communication* Brain-Derived Neurotrophic Factor / metabolism Chronic Disease Humans Hyperoxia / metabolism*, pathology Infant, Newborn Infant, Premature Infant, Premature, Diseases / metabolism*, pathology, therapy Intensive Care Lung / innervation, metabolism* Lung Diseases / metabolism*, pathology, therapy Nerve Growth Factors / metabolism Paracrine Communication* Rats |
| Grant Support | |
ID/Acronym/Agency:
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HL 56470/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Brain-Derived Neurotrophic Factor; 0/Nerve Growth Factors |
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