https://pureadmin.qub.ac.uk/ws/files/16243586/BMP_signalling_Agony_and_Antagony_in_the_family.pdf

BMP signalling: agony and antagony in the family

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.

/pdf/mir-206-inhibits-fn1-expression-and-proliferation-and-1lsqg0iqc1.pdf

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

Pulmonary surfactant (PS), which is synthesized by type II alveolar epithelial cells (AECIIs), maintains alveolar integrity by reducing surface tension. Many premature neonates who lack adequate PS are predisposed to developing respiratory distress syndrome (RDS), one of the leading causes of neonatal morbidity and mortality. PS synthesis is influenced and regulated by various factors, including microRNAs. Previous in vitro studies have shown that PS synthesis is regulated by miR-26a in fetal rat AECIIs. This study aimed to investigate the role of miR-26a in PS synthesis in vivo. To obtain a miR-26a-1/miR-26a-2 double knockout mouse model, we used the clustered regularly interspaced short palindromic repeat/CRISPR-associated protein 9 (CRISPR/Cas9) system, an important genome editing technology. Real-time PCR was performed to determine the miR-26a levels in various organs, as well as the mRNA levels of surfactant-associated proteins. Moreover, AECIIs and surfactant-associated proteins in lung tissues were analyzed by hematoxylin-eosin staining and immunohistochemistry. Homozygous offspring of miR-26a-1/miR-26a-2 double knockout mice generated using the CRISPR/Cas9 system were successfully obtained, and PS synthesis and the number of AECIIs were significantly increased in the miR-26a knockout mice. These results indicate that miR-26a plays an important role in PS synthesis in AECIIs.

Pulmonary surfactant synthesis in miRNA-26a-1/miRNA-26a-2 double knockout mice generated using the CRISPR/Cas9 system.

Normal formation and function of the lungs are essential for the transition of the fetus to an air‑breathing environment at birth. The synthesis of pulmonary surfactant (PS), which is produced by type II alveolar epithelial cells (AECIIs), is required for proper lung development. Previous in vitro studies have suggested that PS synthesis is regulated by microRNA (miR)‑26a in fetal rat AECIIs. The present study explored the potential role of miR‑26a in lung development and PS synthesis by using a miR‑26a‑1/miR‑26a‑2 double knockout mouse model. Hematoxylin and eosin staining and transmission electron microscopy were used to observe the morphology of fetal lungs. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were performed to examine the mRNA and protein levels of surfactant‑associated proteins. The results demonstrated that the lung formation in the knockout mice was more mature, and that there were more mature lamellar bodies inside AECIIs in miR‑26a knockout mice at late stages of lung development. The findings further demonstrated that knockout of miR‑26a increased surfactant‑associated mRNA and protein expression levels. The results indicated that knockout of miR‑26a promotes lung development and PS synthesis.

/pdf/knockout-of-microrna-26a-promotes-lung-development-and-ezst42otpj.pdf

Knockout of microRNA‑26a promotes lung development and pulmonary surfactant synthesis.

The discovery of peripheral intracellular clocks revealed circadian oscillations of clock genes and their targets in all cell types, including those in the lung, sparking exploration of clocks in lung disease pathophysiology. While the focus has been on the role of these clocks in adult airway diseases, clock biology is also likely to be important in perinatal lung development, where it has received far less attention. Historically, fetal circadian rhythms have been considered irrelevant owing to lack of external light exposure, but more recent insights into peripheral clock biology raise questions of clock emergence, its concordance with tissue-specific structure/function, the interdependence of clock synchrony and functionality in perinatal lung development, and the possibility of lung clocks in priming the fetus for postnatal life. Understanding the perinatal molecular clock may unravel mechanistic targets for chronic airway disease across the lifespan. With current research providing more questions than answers, it is about time to investigate clocks in the developing lung.

/pdf/it-s-about-time-clocks-in-the-developing-lung-90q8s979ue.pdf

It's about time: clocks in the developing lung.

Pulmonary surfactant, a unique developmentally regulated, phospholipid-rich lipoprotein, is synthesized by the type II epithelial cells (AECII) of the pulmonary alveolus, where it is stored in organelles termed lamellar bodies. The synthesis of pulmonary surfactant is under multifactorial control and is regulated by a number of hormones and factors, including glucocorticoids, prolactin, insulin, growth factors, estrogens, androgens, thyroid hormones, and catecholamines acting through beta-adrenergic receptors, and cAMP. While there is increasing evidence that microRNAs (miRNAs) are involved in the regulation of almost every cellular and physiological process, the potential role of miRNAs in the regulation of pulmonary surfactant synthesis remains unknown. miRNA-26a (miR-26a) has been predicted to target SMAD1, one of the bone morphogenetic protein (BMP) receptor downstream signaling proteins that plays a key role in differentiation of lung epithelial cells during lung development. In this study, we explored the regulation role of miR-26a in the synthesis of pulmonary surfactant. An adenoviral miR-26a overexpression vector was constructed and introduced into primary cultured fetal AECII. GFP fluorescence was observed to determinate the transfection efficiency and miR-26a levels were measured by RT-PCR. MTT was performed to analyze AECII viability. qRT-PCR and Western blotting were used to determine the mRNA and protein level of SMAD1 and surfactant-associated proteins. The results showed that miR-26a in fetal AECII was overexpressed after the transfection, and that the overexpression of miR-26a inhibited pulmonary surfactant synthesis in AECII. There was no significant change in cell proliferation. Our results further showed that overexpression of miR-26a reduced the SMAD1 expression both in mRNA and protein level in fetal AECII. These findings indicate that miR-26a regulates surfactant synthesis in fetal AECII through SMAD1.

Regulation of pulmonary surfactant synthesis in fetal rat type II alveolar epithelial cells by microRNA-26a.

Exploring spatiotemporal evolution features and factors affecting pollution reduction and carbon abatement on the urban agglomeration scale is helpful to better understand the interaction between ecological environment and economic development in urban agglomerations. In this study, we constructed an evaluation index system for collaborative governance of pollution reduction and carbon abatement in urban agglomerations. In addition, we employed the correlation coefficient matrix, the composite system synergy model, the Gini coefficient, and the Theil index to evaluate the level of and regional differences in collaborative governance of pollution reduction and carbon abatement in seven urban agglomerations in the Yellow River Basin from 2006 to 2020. Moreover, we explored the factors affecting collaborative governance of pollution reduction and carbon abatement in urban agglomerations in the basin. The following findings were obtained: (1) the order degree of collaborative governance of pollution reduction and carbon abatement in the seven urban agglomerations exhibited a significant growing trend, representing a spatial evolution feature of “high in the west and low in the east”; (2) the internal differences in collaborative governance synergy of pollution reduction and carbon abatement decreased in Lanzhou–Xining Urban Agglomeration, Hohhot–Baotou–Ordos–Yulin Urban Agglomeration, Central Shanxi Urban Agglomeration, Zhongyuan Urban Agglomeration, and Shandong Peninsula Urban Agglomeration, while the internal differences basically remained stable in Guanzhong Urban Agglomeration and the Urban Agglomeration along the Yellow River in Ningxia; (3) the variances in environmental regulation and industrial structure among urban agglomerations had a significant positive effect on collaborative governance of pollution reduction and carbon abatement in urban agglomerations in the basin, and the variances in economic growth had a significant inhibitory effect. In addition, the variances in energy consumption, greening construction, and opening-up had an inhibitory impact on collaborative governance of pollution reduction, but the impact was not significant. Finally, this study proposes various recommendations to improve collaborative governance for pollution reduction and carbon abatement in urban agglomerations in the basin in terms of promoting industrial structure upgrading, strengthening regional cooperation, and reducing regional differences. This paper represents an empirical reference for formulating differentiated collaborative governance strategies for pollution reduction and carbon abatement, comprehensive green and low-carbon economic and social transformation programs, and high-quality green development paths in urban agglomerations, which is of certain theoretical and practical significance.

https://www.mdpi.com/1660-4601/20/5/3994/pdf?version=1677146823

Study on Spatiotemporal Evolution Features and Affecting Factors of Collaborative Governance of Pollution Reduction and Carbon Abatement in Urban Agglomerations of the Yellow River Basin

Objective To bioinformatically predict and analyze target genes of miRNA-126(*), with the aim of providing certain basis for related research about target genes and regulatory mechanism in the future. Methods The miRNA chip technology was applied to measure expression levels of miRNA-126(*) in 3 time points (embryo 16, 19 and 21 days) of fetal lung development. Then the target genes of miRNA-126(*) were screened through miRGen2.0 database. Subsequent bioinformatic analysis of these target genes was performed by Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes Pathway analysis (KEGG Pathway analysis). Results miRNA-126(*) manifested continuously upregulated expression with the lung development (from embryo 16 to 21 days). There were 422 predicted target genes in total, and the gene set mainly located in glucuronosyltransferase activity, transferase activity (GO molecular function), multicellular organismal development, developmental process (GO biology process) and intracellular part (GO cellular component). The KEGG Pathway analysis demonstrated that the gene set mostly located in RNA degradation (signal transduction pathway) and prion diseases (disease pathway). Conclusions The results suggest that miRNA-126(*) plays a certain role in fetal lung development and provide a basis for lung development research in the future.

[Bioinformatic analysis of target gene prediction and related signaling pathways of miRNA-126*].

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Pan Zhang

Author Tools

Chat about Author

Papers

Regulation of pulmonary surfactant synthesis in fetal rat type II alveolar epithelial cells by microRNA-26a.

Study on Spatiotemporal Evolution Features and Affecting Factors of Collaborative Governance of Pollution Reduction and Carbon Abatement in Urban Agglomerations of the Yellow River Basin

[Bioinformatic analysis of target gene prediction and related signaling pathways of miRNA-126*].