Mechanisms Of Bronchopulmonary Dysplasia Research Articles

Genome-wide exploration of a pyroptosis-related gene module along with immune cell infiltration patterns in bronchopulmonary dysplasia.

Pyroptosis plays a crucial role in bronchopulmonary dysplasia (BPD) and is associated with various lung injury illnesses. However, the function of pyroptosis-related genes (PRGs) in BPD remains poorly understood. The gene expression omnibus (GEO) database was searched for information on genes associated with BPD. Twenty-five BPD-related DE-PRGs were identified, all of which were closely associated with pyroptosis regulation and immunological response. LASSO and SVM-RFE algorithms identified CHMP7, NLRC4, NLRP2, NLRP6, and NLRP9 among the 25 differentially expressed PRGs as marker genes with acceptable diagnostic capabilities. Using these five genes, we also generated a nomogram with excellent predictive power. Annotation enrichment analyses revealed that these five genes may be implicated in BPD and numerous BPD-related pathways. In addition, the ceRNA network showed an intricate regulatory link based on the marker genes. In addition, CIBERSORT-based studies revealed that alterations in the immunological microenvironment of BPD patients may be associated with the marker genes. We constructed a diagnostic nomogram and gave insight into the mechanism of BPD. Its diagnostic value for BPD must be evaluated in further research before it can be used in clinical practice.

Progress and prospects of biomarkers of bronchopulmonary dysplasia in premature infants

Bronchopulmonary dysplasia(BPD)is one of the most serious lung diseases in premature infants and an important cause of death in preterm infants.The pathophysiological mechanism of BPD is still unclear.The preventive and targeted treatment strategies for this disease are also very limited.However, various biomarkers have been found in blood, alveolar lavage fluid, exhaled gas condensate, and urine.It is used to identify high-risk children with BPD early and to predict the severity and prognosis of the disease. Key words: Biomarker; Bronchopulmonary dysplasia; Premature

Bioinformatic analysis of the molecular mechanism underlying bronchial pulmonary dysplasia using a text mining approach.

Bronchopulmonary dysplasia (BPD) is a common disease of premature infants with very low birth weight. The mechanism is inconclusive. The aim of this study is to systematically explore BPD-related genes and characterize their functions.Natural language processing analysis was used to identify BPD-related genes. Gene data were extracted from PubMed database. Gene ontology, pathway, and network analysis were carried out, and the result was integrated with corresponding database.In this study, 216 genes were identified as BPD-related genes with P < .05, and 30 pathways were identified as significant. A network of BPD-related genes was also constructed with 17 hub genes identified. In particular, phosphatidyl inositol-3-enzyme-serine/threonine kinase signaling pathway involved the largest number of genes. Insulin was found to be a promising candidate gene related with BPD, suggesting that it may serve as an effective therapeutic target.Our data may help to better understand the molecular mechanisms underlying BPD. However, the mechanisms of BPD are elusive, and further studies are needed.

MiR-206 inhibits FN1 expression and proliferation and promotes apoptosis of rat type II alveolar epithelial cells.

Bronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung injury, primarily in preterm infants. miR-206 and fibronectin 1 (FN1) are associated with the development of BPD. The present study used rat type II alveolar epithelial cells (AECII) to investigate the underlying mechanisms of BPD. AECII were isolated using a primary cell culture prior to alkaline phosphatase staining and immunofluorescence of surfactant protein C (SP-C). These were used to verify the presence of AECII. AECII were then divided into four groups, which were transfected with four different plasmids. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the relative expression of miR-206 in the each group. The gene and protein expression level of FN1 was detected by RT-qPCR and immunofluorescence. The proliferation of AECII in each of the four groups was evaluated using an MTT assay 48 h following transfection. The percentage of apoptotic cells was determined by flow cytometric analysis. The present study demonstrated that upregulation of miR-206 decreased the expression of FN1 (P<0.05) and low levels of miR-206 led to increased expression of FN1 (P<0.05) in AECII. Furthermore, the forced expression of miR-206 suppressed proliferation and promoted apoptosis of AECII while downregulation of miR-206 had the opposite effect (P<0.05). The results of the current study provide valuable insights into the prevention of BPD and suggest that miR-206 may be used as a potential molecular target for BPD therapy in the future.

Cell signaling pathways and bronchopulmonary dysplasia

The bronchopulmonary dysplasia(BPD), one of the most common complications in premature infants, has become one of the most difficult problems in neonatal intensive care unit.The molecular mechanism of BPD is extremely complicated, of which the pathogenesis process requires the participation of many signal transduction pathways.This article summarizes the probable relationship of mitogen activated protein kinases signal pathways, nuclear factor-κB pathways, transforming growth factor beta pathways, Wnt pathways, mTOR pathways with BPD. Key words: Cell signaling pathways; Bronchopulmonary dysplasia; Pulmonary fibrosis

Mechanisms of bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting premature infants with long term effect on lung function into adulthood. Multiple factors are involved in the development of BPD. This review will summarize the different mechanisms leading to this disease and highlight recent bench and clinical research targeted at understanding the role of the mesenchyme (both its cellular and extracellular components) in the pathogenesis of BPD.

Adenosine deaminase levels in premature infants with respiratory distress syndrome and bronchopulmonary dysplasia

Adenosine is produced in the inflammed and damaged lung where it plays roles in the regulation of inflammation and tissue remodeling. Adenosine deaminase (ADA) is an enzyme responsible for the degradation of adenosine. Our aim was to compare the levels of ADA between infants with and without respiratory distress syndrome (RDS) and to determine the relationship between plasma ADA levels and bronchopulmonary dysplasia (BPD). One-hundred and twenty-five premature infants who were admitted to our neonatal intensive care unit were included in the study. Eighty-one of these infants with RDS were study group and the other 44 infants without RDS served as controls. Blood collection was made in the first day of life at the end of 24th-h and was used for laboratory testing. In the RDS group, mean ADA level was 25.5 (±4.5) U/l, and in controls it was 26.3 (±5.7) U/l. There was no statistically significant difference (p = 0.326) in these groups although there was a statistically difference of ADA levels between BPD (34.5 ± 5.2 U/l) and non-BPD (24.6 ± 4.1) patients (p = 0.001). There was also a positive relationship between ADA levels and severity of BPD (r = + 0.845, p = 0.01). Perinatal inflammation is the key mechanism of BPD. ADA level in early postnatal life is elevated in infants with BPD and may be related with perinatal inflammation.

Letters to the Editor

In agreement with other authors who have investigated the mechanisms of bronchopulmonary dysplasia (BPD), we have used Bancalari's definition in our recent publication.1,2 However, we certainly agree that from a clinical point of view it is much more appropriate to define the disease when clinical symptoms are present at a corrected age of 36 weeks, as recently stated by Merritt et al.3 Moreover, a more differentiated descriptive definition, as suggested by Weinstein et al,4 could be helpful for the comparison of pulmonary outcomes in clinical trials.