PMID- 16813975
OWN - NLM
STAT- MEDLINE
DCOM- 20061201
LR  - 20151119
IS  - 0146-0005 (Print)
IS  - 0146-0005 (Linking)
VI  - 30
IP  - 3
DP  - 2006 Jun
TI  - Neonatal lung and airway injury: a role for neurotrophins.
PG  - 156-62
AB  - 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.
FAU - Yao, Qin
AU  - Yao Q
AD  - 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.
FAU - Zaidi, Syed I
AU  - Zaidi SI
FAU - Haxhiu, Musa A
AU  - Haxhiu MA
FAU - Martin, Richard J
AU  - Martin RJ
LA  - eng
GR  - HL 56470/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - United States
TA  - Semin Perinatol
JT  - Seminars in perinatology
JID - 7801132
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - *Autocrine Communication
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Chronic Disease
MH  - Critical Care
MH  - Humans
MH  - Hyperoxia/*metabolism/pathology
MH  - Infant, Newborn
MH  - Infant, Premature
MH  - Infant, Premature, Diseases/*metabolism/pathology/therapy
MH  - Lung/innervation/*metabolism
MH  - Lung Diseases/*metabolism/pathology/therapy
MH  - Nerve Growth Factors/metabolism
MH  - *Paracrine Communication
MH  - Rats
RF  - 50
EDAT- 2006/07/04 09:00
MHDA- 2006/12/09 09:00
CRDT- 2006/07/04 09:00
PHST- 2006/07/04 09:00 [pubmed]
PHST- 2006/12/09 09:00 [medline]
PHST- 2006/07/04 09:00 [entrez]
AID - S0146-0005(06)00064-4 [pii]
AID - 10.1053/j.semperi.2006.04.008 [doi]
PST - ppublish
SO  - Semin Perinatol. 2006 Jun;30(3):156-62. doi: 10.1053/j.semperi.2006.04.008.