دورية أكاديمية

Identification of proteins related to SIS3 by iTRAQ and PRM-based comparative proteomic analysis in cisplatin-induced acute kidney injury

التفاصيل البيبلوغرافية
العنوان: Identification of proteins related to SIS3 by iTRAQ and PRM-based comparative proteomic analysis in cisplatin-induced acute kidney injury
المؤلفون: Jiayan Huang, Jian Ye, Yi Gao, Yu Wang, Qing Zhao, Tanqi Lou, Weiyan Lai
المصدر: PeerJ, Vol 12, p e17485 (2024)
بيانات النشر: PeerJ Inc., 2024.
سنة النشر: 2024
المجموعة: LCC:Medicine
LCC:Biology (General)
مصطلحات موضوعية: Acute kidney injury, Fatty acid oxidation, Smad3, N-myc downstream regulated gene 1, Proteomic, Medicine, Biology (General), QH301-705.5
الوصف: Background Cisplatin is a commonly used nephrotoxic drug and can cause acute kidney injury (AKI). In the present study, isobaric tags for relative and absolute quantification (iTRAQ) and parallel reaction monitoring (PRM)-based comparative proteomics were used to analyze differentially expressed proteins (DEPs) to determine the key molecular mechanism in mice with cisplatin-induced AKI in the presence or absence of SIS3, a specific p-smad3 inhibitor, intervention. Methods The cisplatin-induced AKI mouse model was established and treated with SIS3. We used iTRAQ to search for DEPs, PRM to verify key DEPs and combined Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) for bioinformatics analysis. We then assessed lipid deposition, malondialdehyde (MDA) and reactive oxygen species (ROS) and detected the expression of SREBF1, SCD1, CPT1A, PPARα and NDRG1 in vitro. Results Proteomic analysis showed that the identified DEPs were mainly enriched in energy metabolism pathways, especially in lipid metabolism. When SIS3 was applied to inhibit the phosphorylation of Smad3, the expression of NDRG1 and fatty acid oxidation key proteins CPT1A and PPARα increased, the expression of lipid synthesis related proteins SREBF1 and SCD1 decreased and the production of lipid droplets, MDA and ROS decreased. Conclusion SIS3 alleviates oxidative stress, reduces lipid accumulation and promotes fatty acid oxidation through NDRG1 in cisplatin-induced AKI. Our study provides a new candidate protein for elucidating the molecular mechanisms of fatty acid metabolism disorders in cisplatin-induced acute kidney injury.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2167-8359
91208807
Relation: https://peerj.com/articles/17485.pdf; https://peerj.com/articles/17485/; https://doaj.org/toc/2167-8359
DOI: 10.7717/peerj.17485
URL الوصول: https://doaj.org/article/ea25ab97927e488e912088078c1182b2
رقم الأكسشن: edsdoj.25ab97927e488e912088078c1182b2
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:21678359
91208807
DOI:10.7717/peerj.17485