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.

• MeSH
• Cyclooxygenase 2 * metabolism   genetics   MeSH
• Muscle Fibers, Skeletal metabolism   enzymology   pathology   MeSH
• Muscle, Skeletal metabolism   pathology   MeSH
• Cells, Cultured MeSH
• Humans MeSH
• Rotator Cuff Injuries * metabolism   pathology   enzymology   genetics   MeSH
• Cell Proliferation MeSH
• STAT3 Transcription Factor metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Cyclooxygenase 2 * MeSH
• PTGS2 protein, human MeSH Browser
• STAT3 protein, human MeSH Browser
• STAT3 Transcription Factor MeSH

MicroRNAs have been shown to potentially function in cerebral ischemia/reperfusion (IR) injury. This study aimed to examine the expression of microRNA-320 (miR-320) in cerebral IR injury and its involvement in cerebral mitochondrial function, oxidative stress, and inflammatory responses by targeting the HMGB1/NF-kappaB axis. Sprague-Dawley rats were subjected to middle cerebral artery occlusion to simulate cerebral IR injury. The cerebral expression of miR-320 was assessed using qRT-PCR. Neurological function, cerebral infarct volume, mitochondrial function, oxidative stress, and inflammatory cytokines were evaluated using relevant methods, including staining, fluorometry, and ELISA. HMGB1 expression was analyzed through Western blotting. The levels of miR-320, HMGB1, neurological deficits, and cerebral infarction were significantly higher after IR induction. Intracerebral overexpression of miR-320 resulted in substantial neurological deficits, increased infarct volume, elevated levels of 8-isoprostane, NF-kappaBp65, TNF-alpha, IL-1beta, ICAM-1, VCAM-1, and HMGB1 expression. It also promoted the loss of mitochondrial membrane potential and ROS levels while reducing MnSOD and GSH levels. Downregulation of miR-320 and inhibition of HMGB1 activity significantly reversed the outcomes of cerebral IR injury. MiR-320 plays a negative role in regulating cerebral inflammatory/oxidative reactions induced by IR injury by enhancing HMGB1 activity and modulating mitochondrial function.

• MeSH
• Infarction, Middle Cerebral Artery genetics   MeSH
• Rats MeSH
• MicroRNAs * genetics   metabolism   MeSH
• NF-kappa B metabolism   MeSH
• Rats, Sprague-Dawley MeSH
• HMGB1 Protein * genetics   MeSH
• Reperfusion Injury * genetics   prevention & control   metabolism   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Hbp1 protein, rat MeSH Browser
• MicroRNAs * MeSH
• MIRN320 microRNA, rat MeSH Browser
• NF-kappa B MeSH
• HMGB1 Protein * MeSH