Objective: To determine the capability of alveolar fluid clearance and the changes of sodium channel in alveolar type II cells (ATII) in oleic acid-induced acute lung injury.
Methods: Forty four male Sprague-Dawley (SD) rats were randomized into a control group and an acute lung injury (ALI) group, with 22 rats in each group. The ALI model was established by oleic acid. The ATII cells were acutely isolated and purified, and the ATII cellular ultrastructure was observed by transmission electron microscope. In each group, the mRNA expression of 3 epithelial sodium channel (ENaC) subunits in acute isolated ATII cells from 8 rats were detected by reverse transcription-polymerase chain reaction (RT-PCR), while the extravascular lung water (EVLW) content was quantified in 7 rats by gravimetric measurement, and the lung histopathological changes were studies in 7 rats.
Results: In the ALI group, Smith lung injury score (7.6 +/- 0.8) and EVLW (0.80 +/- 0.17) ml were significantly higher than those in the control group [Smith score: (1.1 +/- 0.2), t = -20.859, P < 0.01; EVLW: (0.52 +/- 0.10) ml, t = -3.851, P < 0.01]. The transmission electron microscopic observation showed that there were degeneration, apoptosis, and lamellar body vacuolar changes in the ATII cells from the ALI rats. RT-PCR demonstrated that the alpha-subunit of the ENaC mRNA expression was the highest among the 3 subunits (F = 4.40, P = 0.02). In the ALI group, mRNA expressions of all the 3 ENaC subunits in acutely isolated ATII cells were decreased as compared to those in the control group [alpha-subunit: (51 +/- 9)% vs (82 +/- 7)%, t = 7.61, P < 0.01; beta-subunit: (13 +/- 7)% vs (25 +/- 4)%, t = 4.53, P < 0.01; gamma-subunit: (31 +/- 15)% vs (40 +/- 17)%, t = 3.01, P < 0.05; respectively].
Conclusions: The capacity of alveolar fluid clearance was attenuated in oleic acid-induced acute lung injury. The ENaC subunit mRNA levels of ATII cells were significantly decreased in ALI rats.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
PBAE-PEG based lipid nanoparticles for lung cell-specific gene delivery.
Mol Ther
January 2025
Perinatal Institute, Division of Neonatology, Perinatal and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA. Electronic address:
Exemplified by successful use in COVID-19 vaccination, delivery of modified mRNA encapsulated in lipid nanoparticles provides a framework for treating various genetic and acquired disorders. However, lipid nanoparticles that can deliver mRNA into specific lung cell types have not yet been established. Here, we sought whether poly(®-amino ester)s (PBAE) or PEGylated PBAE (PBAE-PEG) in combination with 4A3-SC8/DOPE/cholesterol/DOTAP lipid nanoparticles (LNP) could deliver mRNA into different types of lung cells in vivo.
View Article and Find Full Text PDFPLAC8 attenuates pulmonary fibrosis and inhibits apoptosis of alveolar epithelial cells via facilitating autophagy.
Commun Biol
January 2025
Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Idiopathic pulmonary fibrosis (IPF) is an irreversible lung condition that progresses over time, which ultimately results in respiratory failure and mortality. In this study, we found that PLAC8 was downregulated in the lungs of IPF patients based on GEO data, in bleomycin (BLM)-induced lungs of mice, and in primary murine alveolar epithelial type II (pmATII) cells and human lung epithelial cell A549 cells. Overexpression of PLAC8 facilitated autophagy and inhibited apoptosis of pmATII cells and A549 cells in vitro.
View Article and Find Full Text PDFLIN28A-dependent lncRNA NEAT1 aggravates sepsis-induced acute respiratory distress syndrome through destabilizing ACE2 mRNA by RNA methylation.
J Transl Med
January 2025
Emergency Department, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510630, China.
Background: Acute respiratory distress syndrome (ARDS) is a life-threatening and heterogeneous disorder leading to lung injury. To date, effective therapies for ARDS remain limited. Sepsis is a frequent inducer of ARDS.
View Article and Find Full Text PDFActivated DRP1 promotes mitochondrial fission and induces glycolysis in ATII cells under hyperoxia.
Respir Res
December 2024
Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Backgroud: Recent studies have reported mitochondrial damage and metabolic dysregulation in BPD, but the changes in mitochondrial dynamics and glucose metabolic reprogramming in ATII cells and their regulatory relationship have not been reported.
Methods: Neonatal rats in this study were divided into model (FIO2:85%) and control (FIO2: 21%) groups. Lung tissues were extracted at 3, 7, 10 and 14 postnatal days and then conducted HE staining for histopathological observation.
Mechanism of miR-130b-3p in relieving airway inflammation in asthma through HMGB1-TLR4-DRP1 axis.
Cell Mol Life Sci
December 2024
Jilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji, 133002, People's Republic of China.
Asthma is a chronic inflammatory respiratory disease characterized by recurrent breathing difficulties caused by airway obstruction and hypersensitivity. Although there is diversity in their specific mechanisms, microRNAs (miRNAs) have a significant impact on the development of asthma. Currently, the contribution of miR-130b-3p to asthma remains elusive.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!