A Comparison of KL-6 and Clara Cell Protein as Markers for Predicting Bronchopulmonary Dysplasia in Preterm Infants

Wang, Keyi; Huang, Xu; Lu, Hui; Zhang, Zuo‐Feng

doi:10.1155/2014/736536

Cited by 21 publications

(22 citation statements)

References 25 publications

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“…Interstitial lung disease is mainly caused by type II lung epithelial cell injury and abnormal accumulation of extracellular matrix in lung parenchyma. Similar pathology is also seen in BPD (Wang et al, 2014). It has been reported that KL-6 level in peripheral blood is closely related to the severity of BPD (Wang et al, 2014;Matsumura et al, 2017).…”

Section: Introductionmentioning

confidence: 57%

“…Similar pathology is also seen in BPD (Wang et al, 2014). It has been reported that KL-6 level in peripheral blood is closely related to the severity of BPD (Wang et al, 2014;Matsumura et al, 2017). Superoxide dismutase (SOD) is required for repairing neovascularization in response to ischemic injury by preventing excessive production of superoxide (Kim et al, 2007).…”

Section: Introductionmentioning

confidence: 57%

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Promotion of Bronchopulmonary Dysplasia Progression Using Circular RNA circabcc4 via Facilitating PLA2G6 Expression by Sequestering miR-663a

Chen

Feng

et al. 2020

Front. Cell Dev. Biol.

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Circular RNA (circRNA) has been increasingly proven as a new type of promising therapeutic RNA molecule in a variety of human diseases. However, the role of circRNA in bronchopulmonary dysplasia (BPD) has not yet been elucidated. Here, a new circRNA circABCC4 was identified from the Agilent circRNA chip as a differentially expressed circRNA in BPD. The relationship between circABCC4 level and BPD clinicopathological characteristics was analyzed. The function of circABCC4 was evaluated by performing CCK-8 and apoptosis analysis in vitro and BPD model analysis in vivo. RNA immunoprecipitation (RIP), luciferase reporter and rescue experiments were used to elucidate the interaction between circABCC4 and miR-663a. Luciferase reporter assay and rescue experiments were used to elucidate the interaction between PLA2G6 and miR-663a. CircABCC4 and PLA2G6 levels were increased, while miR-663a levels were decreased in the BPD group, compared to the control group. MiR-663a inhibited apoptosis by repressing PLA2G6 expression, while circABCC4 enhanced the apoptosis and inhibited the proliferation of A549 cells by sponging miR-663a and increasing PLA2G6 expression. In conclusion, circABCC4 promotes the evolving of BPD by spongening miR-663a and up-regulating PLA2G6 expression, which makes circABCC4 an ideal molecular target for early diagnosis and intervention of BPD.

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Section: Introductionmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 57%

Promotion of Bronchopulmonary Dysplasia Progression Using Circular RNA circabcc4 via Facilitating PLA2G6 Expression by Sequestering miR-663a

Chen

Feng

et al. 2020

Front. Cell Dev. Biol.

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“…They also reported that a plasma level of 199 U/mL at 1 week or 232 U/mL at 2 weeks was an excellent predictor of moderate/ severe BPD (PPV of 83% and 80%, respectively). Wang et al (20) investigated predictive characteristics of KL-6 and Clara cell protein (CC16), another peripheral blood biomarker originating from nonciliated Clara cells, for BPD in preterm infants. They found that serum KL-6 levels higher than 79.26 ng/mL at 14 days postpartum in preterm infants predict the occurrence of BPD.…”

Section: Discussionmentioning

confidence: 99%

Predictive values of plasma KL-6 in bronchopulmonary dysplasia in preterm infants

Díllí¹,

Özyazici²,

Dursun³

et al. 2017

Turk J Med Sci

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IntroductionBronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung parenchymal injury, occurring especially in preterm infants (1). BPD remains a serious problem in very low birthweight (VLBW) infants despite the use of antenatal steroids and postnatal surfactant therapy to decrease the incidence and severity of respiratory distress syndrome (RDS) (2,3). BPD has a complex and multifactorial etiology, including oxygen toxicity, preterm delivery, hypoxia/hyperoxia, infection, and inflammation (4).Many studies have suggested that lung inflammation is a major contributor to the pathogenesis of BPD (5,6). Various parameters of lung inflammation may be used to show lung inflammation. However, most of them such as N-terminal propeptide of type 3 collagen, SP-A, anti-SP-A immune complexes, nitrotyrosine, soluble E-selectin, intercellular adhesion molecule-1, allantoin, and aldehydes are not specific for lung disease or are complicated to measure (6). Krebs yon den Lundgen-6 (KL-6) is a mucinlike high-molecular weight glycoprotein that is classified into cluster 9 (MUC1) of lung tumor and differentiation antigens. It is preferentially expressed by alveolar type 2 cells and stimulates lung fibrosis through its action as a fibroblast chemotactic factor (7).There are many studies suggesting plasma KL-6 is increased in adult patients with various types of interstitial pneumonia, characterized by type 2 alveolar hyperplasia and fibrosis (8-11). KL-6 has also shown to be as a useful marker for increased alveolar vascular permeability associated with lung injury. However, plasma KL-6 levels are not elevated in noninterstitial lung diseases such as bacterial pneumonia, bronchial asthma, and pulmonary emphysema (9). Similar pathological changes seen in interstitial pneumonia in the lung are also predominant in BPD (7,12,13). Plasma KL-6 can be a clinically useful early marker for BPD. However, there are few data on the predictive characteristics of KL-6. Therefore, in the present study, we aimed to evaluate the predictive values of KL-6 in BPD within the first days of life. Materials and methods Study populationAll eligible preterm infants between May 2014 and April 2015 were prospectively enrolled in this study, specifically neonates with birthweight ≤1500 g and gestational age ≤32 Background/aim: It has been suggested that plasma KL-6 increases in premature infants with bronchopulmonary dysplasia (BPD). We aimed to evaluate the predictive values of KL-6 in BPD. Materials and methods:The study was performed in preterm neonates with birthweight ≤1500 g and gestational age ≤32 weeks. Plasma KL-6 levels were measured on postnatal days 1, 7, and 14.Results: BPD was identified in eight of the 28 study infants. On postnatal days 1 and 7, plasma KL-6 levels were similar in infants with BPD [on

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“…However, the results are conflicting. Reports from cord blood and postnatal serum found lower levels of CC16 in patients who went on to develop BPD ( 19 , 29 ), while one study demonstrated elevated postnatal serum levels in mechanically ventilated infants and correlations with progression to BPD ( 30 ). Yet, another study of tracheal aspirates in preterm infants showed instead a correlation with gestational age as well as elevations in the setting of acute infection ( 66 ).…”

Section: Biomarker Subgroupsmentioning

confidence: 99%

“…In that study, KL-6 levels were also correlated with measures of oxygenation, length of ventilation, and LOS. Other pediatric studies have demonstrated elevated serum KL-6 in infants with bronchiolitis ( 36 ) or BPD ( 29 , 114 ), as well as with respiratory complications in severely developmentally disabled children ( 115 ) and in pediatric interstitial lung disease ( 116 ).…”

Section: Biomarker Subgroupsmentioning

confidence: 99%

Biomarkers in Pediatric ARDS: Future Directions

Orwoll

Sapru

2016

Front. Pediatr.

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Acute respiratory distress syndrome (ARDS) is common among mechanically ventilated children and accompanies up to 30% of all pediatric intensive care unit deaths. Though ARDS diagnosis is based on clinical criteria, biological markers of acute lung damage have been extensively studied in adults and children. Biomarkers of inflammation, alveolar epithelial and capillary endothelial disruption, disordered coagulation, and associated derangements measured in the circulation and other body fluids, such as bronchoalveolar lavage, have improved our understanding of pathobiology of ARDS. The biochemical signature of ARDS has been increasingly well described in adult populations, and this has led to the identification of molecular phenotypes to augment clinical classifications. However, there is a paucity of data from pediatric ARDS (pARDS) patients. Biomarkers and molecular phenotypes have the potential to identify patients at high risk of poor outcomes, and perhaps inform the development of targeted therapies for specific groups of patients. Additionally, because of the lower incidence of and mortality from ARDS in pediatric patients relative to adults and lack of robust clinical predictors of outcome, there is an ongoing interest in biological markers as surrogate outcome measures. The recent definition of pARDS provides additional impetus for the measurement of established and novel biomarkers in future pediatric studies in order to further characterize this disease process. This chapter will review the currently available literature and discuss potential future directions for investigation into biomarkers in ARDS among children.

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A Comparison of KL-6 and Clara Cell Protein as Markers for Predicting Bronchopulmonary Dysplasia in Preterm Infants

Cited by 21 publications

References 25 publications

Promotion of Bronchopulmonary Dysplasia Progression Using Circular RNA circabcc4 via Facilitating PLA2G6 Expression by Sequestering miR-663a

Promotion of Bronchopulmonary Dysplasia Progression Using Circular RNA circabcc4 via Facilitating PLA2G6 Expression by Sequestering miR-663a

Predictive values of plasma KL-6 in bronchopulmonary dysplasia in preterm infants

Biomarkers in Pediatric ARDS: Future Directions

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