bronchopulmonary dysplasia/tyrosine

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Anti-sFlt-1 Therapy Preserves Lung Alveolar and Vascular Growth in Antenatal Models of Bronchopulmonary Dysplasia.

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BACKGROUND Pregnancies complicated by antenatal stress, including preeclampsia (PE) and chorioamnionitis (CA), increase the risk for bronchopulmonary dysplasia (BPD) in preterm infants, but biologic mechanisms linking prenatal factors with BPD are uncertain. Levels of sFlt-1 (soluble fms-like

Association of increased cord blood soluble endoglin with the development of bronchopulmonary dysplasia in preterm infants with maternal preeclampsia.

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OBJECTIVE To investigate whether the levels of angiogenic factors in cord blood are associated with the development of bronchopulmonary dysplasia (BPD) in preterm infants with maternal preeclampsia. METHODS This retrospective cohort study included 199 singleton infants (gestational age < 32 weeks),

Mechanical strain increases protein tyrosine phosphorylation in airway smooth muscle cells.

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Mechanical stress contributes to normal structure and function of the lung as well as pathology in such diseases as bronchopulmonary dysplasia and adult respiratory distress syndrome. Stress-related increases in airway smooth muscle (ASM) quantity are reflected in vitro where cultured ASM cells

Impaired lung vascular endothelial growth factor in extremely premature baboons developing bronchopulmonary dysplasia/chronic lung disease.

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BACKGROUND Preterm infants exposed to O2 with mechanical ventilation often develop bronchopulmonary dysplasia (BPD), a form of chronic lung disease (CLD). The pathogenesis of BPD/CLD involves dysmorphic microvasculature and disrupted alveolarization. This may be due to impaired vascular endothelial

Excess soluble vascular endothelial growth factor receptor-1 in amniotic fluid impairs lung growth in rats: linking preeclampsia with bronchopulmonary dysplasia.

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Epidemiological studies have shown that maternal preeclampsia (PE) increases the risk of bronchopulmonary dysplasia (BPD), but the underlying mechanism is unknown. Soluble vascular endothelial growth factor receptor-1 (soluble VEGFR1, known as soluble fms-like tyrosine kinase 1, or sFlt-1), an

Posttranslational modification of β-catenin is associated with pathogenic fibroblastic changes in bronchopulmonary dysplasia.

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Bronchopulmonary dysplasia (BPD) is a common complication of premature birth. The histopathology of BPD is characterized by an arrest of alveolarization with fibroblast activation. The Wnt/β-catenin signaling pathway is important in early lung development. When Wnt signaling is active,

Is the fibroblast growth factor signaling pathway a victim of receptor tyrosine kinase inhibition in pulmonary parenchymal and vascular remodeling?

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Idiopathic pulmonary arterial hypertension (IPAH), pulmonary hypertension (PH) due to lung disease and/or hypoxia and idiopathic pulmonary fibrosis (IPF) are increasingly recognized as important contributors to mortality and morbidity worldwide. Among others, the current treatment paradigm considers

Angiogenic Factors in Cord Blood of Preterm Infants Predicts Subsequently Developing Bronchopulmonary Dysplasia.

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Bronchopulmonary dysplasia (BPD) of prematurity is associated with impaired angiogenesis. Excess soluble fms-like tyrosine kinase-1 (sFlt-1) and lower levels of vascular endothelial growth factor (VEGF) impaired alveolarization in preterm rats. Overexpression of placenta growth factor (PlGF) in mice

Bronchopulmonary dysplasia and oxidative stress: are we closer to an understanding of the pathogenesis of BPD?

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In recent years a body of data has accumulated, linking the development of bronchopulmonary dysplasia (BPD) to increased oxidative stress in the first few days after birth, since high concentrations of metabolites reflecting increased peroxidation products such as pentane, ethane, protein carbonyl,

A Shared Pattern of β-Catenin Activation in Bronchopulmonary Dysplasia and Idiopathic Pulmonary Fibrosis.

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Wnt/β-catenin signaling is necessary for normal lung development, and abnormal Wnt signaling contributes to the pathogenesis of both bronchopulmonary dysplasia (BPD) and idiopathic pulmonary fibrosis (IPF), fibrotic lung diseases that occur during infancy and aging, respectively. Using a library of

Changes in the plasma aminogram of parenterally fed infants treated with dexamethasone for bronchopulmonary dysplasia.

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A substantial increase in the plasma concentration of most amino acids was observed in 59 preterm infants with chronic lung disease soon after the initiation of dexamethasone therapy. The size of increase appeared to be dose related. This phenomenon is likely to be the result of steroid induced

Dexamethasone increases plasma amino acid concentrations in bronchopulmonary dysplasia.

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Nine ventilated low birthweight babies were treated with dexamethasone (0.6 mg/kg/day). Appreciable suppression of weight gain was accompanied by uraemia and significant increases in the concentration of all amino acids except phenylalanine, tyrosine, threonine, and glutamate. Ornithine, citrulline,

Therapeutic effects of hypercapnia on chronic lung injury and vascular remodeling in neonatal rats.

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Permissive hypercapnia, achieved using low tidal volume ventilation, has been an effective protective strategy in patients with acute respiratory distress syndrome. To date, no such protective effect has been demonstrated for the chronic neonatal lung injury, bronchopulmonary dysplasia. The

Inhaled nitric oxide prevents 3-nitrotyrosine formation in the lungs of neonatal mice exposed to >95% oxygen.

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Inhaled nitric oxide is being evaluated as a preventative therapy for patients at risk for bronchopulmonary dysplasia (BPD). Nitric oxide (NO), in the presence of superoxide, forms peroxynitrite, which reacts with tyrosine residues on proteins to form 3-nitrotyrosine (3-NT). However, NO can also act

Epidermal growth factor receptor in mice and men--any applications to clinical practice?

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The epidermal growth factor receptor (EGF-R) is perhaps the best studied member of tyrosine kinase receptors. Its inactivation by homologous recombination results in three different phenotypes ranging from peri-implantation lethality to postnatal lethality. The mildest form of EGF-R inactivation

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