Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia

Christiana W. Davis, Linda W. Gonzales, Roberta A. Ballard, Philip L. Ballard, Changjiang Guo, Andrew J. Gow

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Bronchopulmonary dysplasia (BPD), a multifactorial disease of preterm neonates of complex etiology, is a significant problem within very low birth weight infants. Nitric oxide (NO) has been implicated in both the pathogenesis and as a potential therapeutic of this disease. At this time, there is little direct evidence of the changes in NO production and metabolism that occur within BPD in humans. Animal models have implied that reduced nitric oxide synthase (NOS) expression and NO production in the early stages of the disease may be critical factors. However, inflammation and hence iNOS expression, is also thought to play a role. In the present study we have utilized pathological samples to determine changes in the expression of NOS and NO metabolites within late stage BPD. It is our contention that within these samples iNOS expression is increased and associated with increased NO metabolite production. Mild immunostaining of all three nitric oxide synthase (NOS) enzymes (neuronal, inducible and endothelial) is observed in control lung with tight localization to the endothelium and epithelial airway. This tight localization was lost in samples from subjects with BPD. There was also a marked increase in iNOS expression throughout the lung tissue with strong coexistence with an epithelial cell marker cytokeratin. NO reaction products are altered with BPD as evidenced by increased S-nitrosothiol (SNO) and strong nitrotyrosine (NO2Y) imunoreactivity. This study demonstrates a strong correlation between products of NO reactivity and NOS localization in BPD.

Original languageEnglish
Pages (from-to)703-709
Number of pages7
JournalPediatric Pulmonology
Volume43
Issue number7
DOIs
Publication statusPublished - Jul 2008
Externally publishedYes

Fingerprint

Bronchopulmonary Dysplasia
Nitric Oxide Synthase
Nitric Oxide
S-Nitrosothiols
Lung
Nitric Oxide Synthase Type I
Very Low Birth Weight Infant
Nitric Oxide Synthase Type III
Keratins
Endothelium
Animal Models
Epithelial Cells
Newborn Infant
Inflammation
Enzymes

Keywords

  • Bronchopulmonary dysplasia
  • Chronic lung disease
  • Inflammation
  • Nitrotyrosine
  • S-nitrosothiol

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Pulmonary and Respiratory Medicine

Cite this

Davis, C. W., Gonzales, L. W., Ballard, R. A., Ballard, P. L., Guo, C., & Gow, A. J. (2008). Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia. Pediatric Pulmonology, 43(7), 703-709. https://doi.org/10.1002/ppul.20848

Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia. / Davis, Christiana W.; Gonzales, Linda W.; Ballard, Roberta A.; Ballard, Philip L.; Guo, Changjiang; Gow, Andrew J.

In: Pediatric Pulmonology, Vol. 43, No. 7, 07.2008, p. 703-709.

Research output: Contribution to journalArticle

Davis, CW, Gonzales, LW, Ballard, RA, Ballard, PL, Guo, C & Gow, AJ 2008, 'Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia', Pediatric Pulmonology, vol. 43, no. 7, pp. 703-709. https://doi.org/10.1002/ppul.20848
Davis, Christiana W. ; Gonzales, Linda W. ; Ballard, Roberta A. ; Ballard, Philip L. ; Guo, Changjiang ; Gow, Andrew J. / Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia. In: Pediatric Pulmonology. 2008 ; Vol. 43, No. 7. pp. 703-709.
@article{2608911b2cae4ba8a55fec544075b43c,
title = "Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia",
abstract = "Bronchopulmonary dysplasia (BPD), a multifactorial disease of preterm neonates of complex etiology, is a significant problem within very low birth weight infants. Nitric oxide (NO) has been implicated in both the pathogenesis and as a potential therapeutic of this disease. At this time, there is little direct evidence of the changes in NO production and metabolism that occur within BPD in humans. Animal models have implied that reduced nitric oxide synthase (NOS) expression and NO production in the early stages of the disease may be critical factors. However, inflammation and hence iNOS expression, is also thought to play a role. In the present study we have utilized pathological samples to determine changes in the expression of NOS and NO metabolites within late stage BPD. It is our contention that within these samples iNOS expression is increased and associated with increased NO metabolite production. Mild immunostaining of all three nitric oxide synthase (NOS) enzymes (neuronal, inducible and endothelial) is observed in control lung with tight localization to the endothelium and epithelial airway. This tight localization was lost in samples from subjects with BPD. There was also a marked increase in iNOS expression throughout the lung tissue with strong coexistence with an epithelial cell marker cytokeratin. NO reaction products are altered with BPD as evidenced by increased S-nitrosothiol (SNO) and strong nitrotyrosine (NO2Y) imunoreactivity. This study demonstrates a strong correlation between products of NO reactivity and NOS localization in BPD.",
keywords = "Bronchopulmonary dysplasia, Chronic lung disease, Inflammation, Nitrotyrosine, S-nitrosothiol",
author = "Davis, {Christiana W.} and Gonzales, {Linda W.} and Ballard, {Roberta A.} and Ballard, {Philip L.} and Changjiang Guo and Gow, {Andrew J.}",
year = "2008",
month = "7",
doi = "10.1002/ppul.20848",
language = "English",
volume = "43",
pages = "703--709",
journal = "Pediatric Pulmonology",
issn = "8755-6863",
publisher = "Wiley-Liss Inc.",
number = "7",

}

TY - JOUR

T1 - Expression of nitric oxide synthases and endogenous NO metabolism in bronchopulmonary dysplasia

AU - Davis, Christiana W.

AU - Gonzales, Linda W.

AU - Ballard, Roberta A.

AU - Ballard, Philip L.

AU - Guo, Changjiang

AU - Gow, Andrew J.

PY - 2008/7

Y1 - 2008/7

N2 - Bronchopulmonary dysplasia (BPD), a multifactorial disease of preterm neonates of complex etiology, is a significant problem within very low birth weight infants. Nitric oxide (NO) has been implicated in both the pathogenesis and as a potential therapeutic of this disease. At this time, there is little direct evidence of the changes in NO production and metabolism that occur within BPD in humans. Animal models have implied that reduced nitric oxide synthase (NOS) expression and NO production in the early stages of the disease may be critical factors. However, inflammation and hence iNOS expression, is also thought to play a role. In the present study we have utilized pathological samples to determine changes in the expression of NOS and NO metabolites within late stage BPD. It is our contention that within these samples iNOS expression is increased and associated with increased NO metabolite production. Mild immunostaining of all three nitric oxide synthase (NOS) enzymes (neuronal, inducible and endothelial) is observed in control lung with tight localization to the endothelium and epithelial airway. This tight localization was lost in samples from subjects with BPD. There was also a marked increase in iNOS expression throughout the lung tissue with strong coexistence with an epithelial cell marker cytokeratin. NO reaction products are altered with BPD as evidenced by increased S-nitrosothiol (SNO) and strong nitrotyrosine (NO2Y) imunoreactivity. This study demonstrates a strong correlation between products of NO reactivity and NOS localization in BPD.

AB - Bronchopulmonary dysplasia (BPD), a multifactorial disease of preterm neonates of complex etiology, is a significant problem within very low birth weight infants. Nitric oxide (NO) has been implicated in both the pathogenesis and as a potential therapeutic of this disease. At this time, there is little direct evidence of the changes in NO production and metabolism that occur within BPD in humans. Animal models have implied that reduced nitric oxide synthase (NOS) expression and NO production in the early stages of the disease may be critical factors. However, inflammation and hence iNOS expression, is also thought to play a role. In the present study we have utilized pathological samples to determine changes in the expression of NOS and NO metabolites within late stage BPD. It is our contention that within these samples iNOS expression is increased and associated with increased NO metabolite production. Mild immunostaining of all three nitric oxide synthase (NOS) enzymes (neuronal, inducible and endothelial) is observed in control lung with tight localization to the endothelium and epithelial airway. This tight localization was lost in samples from subjects with BPD. There was also a marked increase in iNOS expression throughout the lung tissue with strong coexistence with an epithelial cell marker cytokeratin. NO reaction products are altered with BPD as evidenced by increased S-nitrosothiol (SNO) and strong nitrotyrosine (NO2Y) imunoreactivity. This study demonstrates a strong correlation between products of NO reactivity and NOS localization in BPD.

KW - Bronchopulmonary dysplasia

KW - Chronic lung disease

KW - Inflammation

KW - Nitrotyrosine

KW - S-nitrosothiol

UR - http://www.scopus.com/inward/record.url?scp=46849121401&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=46849121401&partnerID=8YFLogxK

U2 - 10.1002/ppul.20848

DO - 10.1002/ppul.20848

M3 - Article

VL - 43

SP - 703

EP - 709

JO - Pediatric Pulmonology

JF - Pediatric Pulmonology

SN - 8755-6863

IS - 7

ER -