Background: Chronic obstructive pulmonary disease (COPD) is a familiar disease, and owns high morbidity and mortality, which critically damages the health of patients. Ubiquitin-specific peptidase 8 (USP8) is a pivotal protein to join in the regulation of some diseases. In a previous report, it was determined that USP8 expression is down-regulated in LPS-treated BEAS-2B cells, and USP8 restrains inflammatory response and accelerates cell viability. However, the regulatory roles of USP8 on ferroptosis in COPD are rarely reported, and the associated molecular mechanisms keep vague.
Objective: To investigate the regulatory functions of USP8 in COPD progression.
Material And Methods: The lung functions were measured through the Buxco Fine Pointe Series Whole Body Plethysmography (WBP). The Fe level was tested through the Fe assay kit. The protein expressions were assessed through western blot. The levels of tumor necrosis -factor-α, interleukin 6, and interleukin 8 were evaluated through enzyme-linked immunosorbent serologic assay. Cell viability was tested through CCK-8 assay.
Results: In this work, it was discovered that overexpression of USP8 improved lung function in COPD mice. In addition, overexpression of USP8 repressed ferroptosis by regulating glutathione peroxidase 4 and acyl-CoA synthetase long-chain family 4 expressions in COPD mice. Overexpression of USP8 suppressed inflammation in COPD mice. Furthermore, overexpression of USP8 suppressed ferroptosis in COPD cell model. At last, it was verified that overexpression of USP8 accelerated ubiquitin aldehyde-binding protein 1 (OTUB1)/solute carrier family 7 member 11 (SLC7A11) pathway.
Conclusion: This study manifested that overexpression of USP8 restrained inflammation and ferroptosis in COPD by regulating the OTUB1/SLC7A11 signaling pathway. This discovery hinted that USP8 could be a potential target for COPD treatment.
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http://dx.doi.org/10.15586/aei.v52i4.1108 | DOI Listing |
Thorac Cancer
January 2025
Department of Cardiothoracic Surgery, The First Affiliated Hospital of Hainan Medical College, Haikou, China.
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December 2024
Xiangya International Academy of Translational Medicine, Central South University, Tongzipo Road, #172, Yuelu District, Changsha, Hunan, 410013, China.
Background: Universal stress proteins (USPs) are prevalent in various bacteria to cope with different adverse stresses, while their possible effects on secondary metabolisms of hosts are unclear. Tiancimycins (TNMs) are ten-membered endiynes possessing excellent potential for development of anticancer antibody-drug conjugates. During our efforts to improve TNMs titer, a high-producing strain Streptomyces sp.
View Article and Find Full Text PDFThorac Cancer
January 2025
Department of Respiratory, Fuzong Clinical Medical College of Fujian Medical University/The 900th Hospital of Joint Logistic Support Force, PLA, Fuzhou, China.
Background: Protein tyrosine kinase 7 (PTK7) has been found to be highly expressed in non-small cell lung cancer (NSCLC), but its specific molecular mechanism needs to be further explored.
Methods: PTK7 mRNA expression in NSCLC tumor tissues was examined by quantitative real-time PCR. The protein levels of PTK7, ubiquitin-specific peptidase 8 (USP8), PIK3CB, and PI3K/AKT were determined by western blot.
Vet Microbiol
November 2024
College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang 453003, China. Electronic address:
Porcine reproductive and respiratory syndrome virus (PRRSV) is an important RNA virus that has caused huge economic losses to swine industry in the whole world. Ubiquitin specific protease 8 (USP8), a pivotal regulator of protein degradation, intricately contributes to orchestrating the delicate balance of various biological processes through its deubiquitinating activity. However, the role of USP8 in antiviral immune response to PRRSV remains elusive.
View Article and Find Full Text PDFAm J Surg Pathol
August 2024
Department of Pathology, Timone University Hospital, Marseille.
Recently, FN1 fusions to receptor tyrosine kinase genes have been identified in soft tissue tumors with calcified chondroid matrix named calcifying chondroid mesenchymal neoplasms (CCMNs). We collected 33 cases of CCMN from the French network for soft tissue and bone tumors. We performed whole-exome RNA sequencing, expression analysis, and genome-wide DNA methylation profiling in 33, 30, and 20 cases of CCMN compared with a control group of tumors, including noncalcified tenosynovial giant cell tumor (TGCT).
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