Altered Urinary Excretion of Elastin Cross-Links in Premature Infants Who Develop Bronchopulmonary Dysplasia

Bruce, Margaret C.; Wedig, Kathy E.; Jentoft, Neil; Martin, Richard J.; Cheng, Pi-Wan; Boat, Thomas F.; Fanaroff, Avroy A.

doi:10.1164/arrd.1985.131.4.568

Cited by 71 publications

(10 citation statements)

References 14 publications

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“…Moreover, markers of fibrosis such as hydroxyproline, fibronectin, and desmosine were increased in lung tissue, tracheal fluid, and urine of preterm infants who developed BPD (23-25). TGF-β has been known to be an important mediator of fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Decreased Expression of Transforming Growth Factor-beta1 in Bronchoalveolar Lavage Cells of Preterm Infants with Maternal Chorioamnionitis

et al. 2008

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Maternal chorioamnionitis has been associated with abnormal lung development. We examined the effect of maternal chorioamnionitis on the expression of transforming growth factor-beta1 (TGF-β1) in the lungs of preterm infants. A total of 63 preterm (≤34 weeks) infants who were intubated in the delivery room were prospectively enrolled. Their placentas were examined for the presence of chorioamnionitis. Bronchoalveolar lavage (BAL) fluid and cells were obtained shortly after birth. TGF-β1 was measured in BAL fluid and TGF-β1 mRNA expression was determined by reverse transcription polymerase chain reaction (RT-PCR) in BAL cells. TGF-β1 mRNA expression in BAL cells showed a positive correlation with gestational age (r=0.414, p =0.002). TGF-β1 mRNA expression was significantly decreased in the presence of maternal chorioamnionitis (0.70±0.12 vs. 0.81±0.15, p =0.007). Adjustment for gestational age, birth weight, and delivery mode did not nullify the significance. TGF-β1 mRNA expression was marginally significantly decreased in preterm infants who developed bronchopulmonary dysplasia (BPD) later (0.75±0.11 vs. 0.82±0.15, p =0.055). However, adjustment for gestational age, patent ductus arteriosus (PDA), and maternal chorioamnionitis nullified the significance. These results might be an indirect evidence that maternal chorioamnionitis may inhibit normal lung development of fetus.

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Section: Discussionmentioning

confidence: 99%

Decreased Expression of Transforming Growth Factor-beta1 in Bronchoalveolar Lavage Cells of Preterm Infants with Maternal Chorioamnionitis

et al. 2008

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“…Data from clinical studies prove the association between the extent of the pulmonary inflammation and the increase in elastase activity in the tracheal aspirates of preterm infants later developing severe BPD. The elastin breakdown products like desmosine can be detected in higher levels in the urine of preterms developing severe BPD and may serve as early markers of disease progression [ 41 , 42 ].…”

Section: The Pulmonary Inflammatory Responsementioning

confidence: 99%

Pathogenesis of bronchopulmonary dysplasia: when inflammation meets organ development

et al. 2016

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Bronchopulmonary dysplasia is a chronic lung disease of preterm infants. It is caused by the disturbance of physiologic lung development mainly in the saccular stage with lifelong restrictions of pulmonary function and an increased risk of abnormal somatic and psychomotor development. The contributors to this disease’s entity are multifactorial with pre- and postnatal origin. Central to the pathogenesis of bronchopulmonary is the induction of a massive pulmonary inflammatory response due to mechanical ventilation and oxygen toxicity. The extent of the pro-inflammatory reaction and the disturbance of further alveolar growth and vasculogenesis vary largely and can be modified by prenatal infections, antenatal steroids, and surfactant application.This minireview summarizes the important recent research findings on the pulmonary inflammatory reaction obtained in patient cohorts and in experimental models. Unfortunately, recent changes in clinical practice based on these findings had only limited impact on the incidence of bronchopulmonary dysplasia.

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“…Examinations of autopsy material from patients that have died with BPD have formed the basis of hypotheses about pathogenic processes at play that limit alveolarization. These observations include (i) severe disturbances to the development of the pulmonary vasculature ( 18 ), (ii) changes in the cellular structure and composition of the developing alveolar units, (iii) increased proteolysis in the alveolar compartments, (iv) increased inflammatory cell infiltration, (v) deregulated growth factor signaling, and (vi) perturbations to the ECM architecture of the developing lung: most notably, the abundance and organization of collagen and elastin fibers ( 19 – 22 ). These disturbances have also been noted in animal models of BPD ( 23 , 24 ).…”

Section: Bronchopulmonary Dysplasia In Contextmentioning

confidence: 99%

The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source

Mižíková

Morty

2015

Front. Med.

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Bronchopulmonary dysplasia (BPD) is a common complication of preterm birth that contributes significantly to morbidity and mortality in neonatal intensive care units. BPD results from life-saving interventions, such as mechanical ventilation and oxygen supplementation used to manage preterm infants with acute respiratory failure, which may be complicated by pulmonary infection. The pathogenic pathways driving BPD are not well-delineated but include disturbances to the coordinated action of gene expression, cell–cell communication, physical forces, and cell interactions with the extracellular matrix (ECM), which together guide normal lung development. Efforts to further delineate these pathways have been assisted by the use of animal models of BPD, which rely on infection, injurious mechanical ventilation, or oxygen supplementation, where histopathological features of BPD can be mimicked. Notable among these are perturbations to ECM structures, namely, the organization of the elastin and collagen networks in the developing lung. Dysregulated collagen deposition and disturbed elastin fiber organization are pathological hallmarks of clinical and experimental BPD. Strides have been made in understanding the disturbances to ECM production in the developing lung, but much still remains to be discovered about how ECM maturation and turnover are dysregulated in aberrantly developing lungs. This review aims to inform the reader about the state-of-the-art concerning the ECM in BPD, to highlight the gaps in our knowledge and current controversies, and to suggest directions for future work in this exciting and complex area of lung development (patho)biology.

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Altered Urinary Excretion of Elastin Cross-Links in Premature Infants Who Develop Bronchopulmonary Dysplasia

Cited by 71 publications

References 14 publications

Decreased Expression of Transforming Growth Factor-beta1 in Bronchoalveolar Lavage Cells of Preterm Infants with Maternal Chorioamnionitis

Decreased Expression of Transforming Growth Factor-beta1 in Bronchoalveolar Lavage Cells of Preterm Infants with Maternal Chorioamnionitis

Pathogenesis of bronchopulmonary dysplasia: when inflammation meets organ development

The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source

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