Bone morphogenetic protein-7 (BMP-7) plays an important role in the epithelial-mesenchymal transition (EMT) process, and has been identified as the most potent factor that can promote mesenchymal-epithelial transition (MET) and reduce organ fibrosis. Here we examined the important role of BMP-7 in silica-induced EMT and investigated the relationship between BMP-7 and the balance of EMT/MET. We found that silica induced EMT and decreased the expression of BMP-7 and , while silica activated the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells. Lentivirus mediated transfection was used to stably upregulate the expression of BMP-7. Exogenous BMP-7 brought on MET exceeded silica-induced EMT and restrained the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells. Our results revealed that BMP-7 promoted MET above EMT induced by silica associated with inhibition of the p38 MAPK/transcription factor signaling pathway, and BMP-7 was a potential target for treatment of silicosis fibrosis.
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http://dx.doi.org/10.1039/c5tx00471c | DOI Listing |
Intensive Care Med Exp
January 2025
Intensive Care Unit, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, 530021, Guangxi, China.
Background: Sepsis-induced acute lung injury (S-ALI) significantly contributes to unfavorable clinical outcomes. Emerging evidence suggests a novel role for ferroptosis in the pathophysiology of ALI, though the precise mechanisms remain unclear. Mild hypothermia (32-34 °C) has been shown to inhibit inflammatory responses, reduce oxidative stress, and regulate metabolic processes.
View Article and Find Full Text PDFChem Biol Interact
January 2025
Hebei Key Laboratory of Organ Fibrosis, School of Public Health, North China University of Science and Technology, Tangshan, Hebei, 063210, China. Electronic address:
Epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of silicosis. High mobility group box 1 (HMGB1) has been found to induce EMT in fibrotic diseases. Previous studies have revealed a critical role of HMGB1 in silicosis, whereas the detail mechanisms still obscure.
View Article and Find Full Text PDFRespir 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.
Cell Mol Life Sci
October 2024
Department of Pulmonary and Critical Care Medicine, Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, 100029, China.
In patients with sepsis, neutrophil apoptosis tends to be inversely proportional to the severity of sepsis, but its mechanism is not yet clear. This study aimed to explore the mechanism of fatty acid binding protein 4 (FABP4) regulating neutrophil apoptosis through combined analysis of gut microbiota and short-chain fatty acids (SCFAs) metabolism. First, neutrophils from bronchoalveolar lavage fluid (BALF) of patients with sepsis-induced acute respiratory distress syndrome (ARDS) were purified and isolated RNA was applied for sequencing.
View Article and Find Full Text PDFOpen Life Sci
August 2024
Pediatric Intensive Care Unit, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, No. 318, Renmin Middle Road, Yuexiu District, Guangzhou, Guangdong, 510120, China.
Sepsis-induced acute lung injury is associated with lung epithelial cell injury. This study analyzed the role of the antimicrobial peptide LL37 with mitochondrial DNA (LL37-mtDNA) and its potential mechanism of action in lipopolysaccharide (LPS)-treated rat type II alveolar epithelial cells (RLE-6TN cells). RLE-6TN cells were treated with LPS alone or with LL37-mtDNA, followed by transcriptome sequencing.
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