ABSTRACT
In sports medicine, injuries related to the insertion of tendons into bones, including rotator cuff injuries, anterior cruciate ligament injuries and Achilles tendon ruptures, are commonly observed. However, traditional therapies have proven to be insufficient in achieving satisfactory outcomes due to the intricate anatomical structure associated with these injuries. Adult bone marrow mesenchymal stem cells possess selfrenewal and multidirectional differentiation potential and can generate various mesenchymal tissues to aid in the recovery of bone, cartilage, adipose tissue and bone marrow hematopoietic tissue. In addition, extracellular vesicles derived from bone marrow mesenchymal stem cells known as exosomes, contain lipids, proteins and nucleic acids that govern the tissue microenvironment, facilitate tissue repair and perform various biological functions. Studies have demonstrated that bone marrow mesenchymal stem cellderived exosomes can function as natural nanocapsules for drug delivery and can enhance tendonbone healing strength. The present review discusses the latest research results on the role of exosomes released by bone marrow mesenchymal stem cells in tendonbone healing and provides valuable information for implementing these techniques in regenerative medicine and sports health.
Subject(s)
Exosomes , Mesenchymal Stem Cells , Rotator Cuff Injuries , Humans , Tendons , Rotator Cuff Injuries/therapy , Wound HealingABSTRACT
Circular RNAs (circRNAs), a type of non-coding RNAs derived from back-splicing, have been reported to function as gene expression regulators involved in tumor development of multiple human tumors. However, the clinical significance and underlying molecular mechanisms of circ_001569 in osteosarcoma still be unknown. In the study, we found that circ_001569 expression was significantly overexpressed in osteosarcoma tissues compared with adjacent noncancerous bone tissues. Higher circ_001569 expression significantly correlated with distant metastasis and advanced tumor stage of osteosarcoma patients. Gain-function and loss-function assays showed that circ_001569 knockdown significantly inhibited osteosarcoma cell proliferation and cell colon formation capacities. Moreover, upregulation of circ_001569 significantly promoted osteosarcoma cell resistance to cisplatin by activating Wnt/ß-catenin signaling pathway. Thus, these results indicated that circ_001569 represented a novel potentially therapeutic target of osteosarcoma.
ABSTRACT
Osteosarcoma is the most common type of malignant tumor arising from bone in children and adolescents. Accumulating evidences have shown the aberrant expression of numerous miRNAs is associated with the development and metastasis of osteosarcoma. The present study was conducted to investigate miR-27a expression in osteosarcoma tissues and cells. In the present study, quantitative RT-qPCR was used to measure the expression levels of miRNA and mRNA in osteosarcoma tissues and cells. Transwell assays were used to detect the effects of miR-27a on the invasive and migratory potential of cells. Luciferase reporter and western blot analysis were conducted to confirm cyclin G1 (CCNG1) as the target gene of miR-27a. The results showed that miR-27a was significantly upregulated in human osteosarcoma tissues and cell lines. The western blot analysis revealed that the overexpression of miR-27a suppressed CCNG1 protein expression. Luciferase reporter assays confirmed that CCNG1 is a direct target of miR-27a in osteosarcoma cells. The results suggest that miR-27a downregulates CCNG1 expression in osteosarcoma and acts as an oncogene directly targeting CCNG1. Thus, the miR-27a/CCNGI axis is a potential therapeutic target for human osteosarcoma.
ABSTRACT
The present study aimed to investigate the anti-inflammatory effects and the underlying molecular mechanism of farrerol on IL-1ß-stimulated human osteoarthritis chondrocytes. Chondrocytes were pretreated with farrerol 1h before IL-1ß stimulation. The effects of farrerol on NO and PGE2 production were tested by Griess reagent and ELISA. The effects of farrerol on COX-2, iNOS, Akt, phosphorylated Akt, and NF-κB activation were measured by western blot analysis. The results showed that farrerol remarkably inhibited IL-1ß-induced NO and PGE2 production, as well as COX-2 and iNOS expression. Farrerol also inhibited IL-1ß-induced NF-κB activation. Furthermore, farrerol significantly inhibited IL-1ß-induced phosphorylation of PI3K and Akt. In conclusion, these results indicated that farrerol inhibited IL-1ß-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-κB signaling pathway.
