Mechanistic Studies of Cyclooxygenase-2 (COX-2) in Skeletal Muscle Cells During Rotator Cuff Injury: An In Vitro Study
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
39545791
PubMed Central
PMC11629944
DOI
10.33549/physiolres.935282
PII: 935282
Knihovny.cz E-zdroje
- MeSH
- cyklooxygenasa 2 * metabolismus genetika MeSH
- kosterní svalová vlákna metabolismus enzymologie patologie MeSH
- kosterní svaly metabolismus patologie MeSH
- kultivované buňky MeSH
- lidé MeSH
- poranění rotátorové manžety * metabolismus patologie enzymologie genetika MeSH
- proliferace buněk MeSH
- transkripční faktor STAT3 metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- cyklooxygenasa 2 * MeSH
- PTGS2 protein, human MeSH Prohlížeč
- STAT3 protein, human MeSH Prohlížeč
- transkripční faktor STAT3 MeSH
The mechanism of rotator cuff injury remains to be elucidated. And COX-2 plays a dual role in skeletal muscle injury and regeneration, would be associated with the development of rotator cuff injury. Therefore, we chose human skeletal muscle cells (HSKMC) as an in vitro muscle tissue model and transfected lentivirus with overexpressed COX-2 to simulate the in vitro environment of rotator cuff injury. To investigate the specific molecular biological mechanism of COX-2, transcriptome sequencing (RNA-Seq) was used to analyze the differentially expressed mRNAs in HSKMC overexpressing COX-2. Enrichment analysis was performed to analyze these differentially expressed genes and real-time quantitative PCR (RT-qPCR) was used to examine the mRNA levels of genes induced by overexpression. Subsequently, the role of COX-2 in cell proliferation was confirmed by cell counting kit-8 (CCK-8), and focal adhesion kinase (FAK) and signal transducer and activator of transcription 3 (STAT3) phosphorylation induced by COX-2 was utilized by western blotting (WB). The results showed that total of 30,759 differentially expressed genes were obtained, and the expression of CYP4F3 and GPR87 was significantly increased. COX-2 could bind CYP4F3 and GPR87 and co-localize with them in the cytoplasm. Finally, COX-2 promoted the proliferation of human skeletal muscle cells by activating the FAK and STAT3 pathways.
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