EDNRB is Upregulated in Acutely Injured Cartilage following Topical Administration of Tranexamic Acid in Rats

This is the authors' abstract. We don't add key points for this paper.

Objective The intra-articular injection of tranexamic acid (TXA) has been shown to be effective at reducing perioperative bleeding. However, the damage to human articular cartilage caused by TXA could contribute to posttraumatic osteoarthritis (PTOA) after acute cartilage injury. In the present study, we aimed to investigate the genes and molecular programmes controlling PTOA pathogenesis associated with TXA using RNA sequencing (RNA-seq). Methods We performed RNA-seq and computational analyses of cartilage tissues obtained from various groups of rats. The differentially expressed genes between the control group and each experimental group were collated to identify those genes that were regulated by TXA. We investigated the role of TXA in cartilage tissue degeneration using RT‒qPCR analysis and histological assays. Results We identified 3113 genes (1834 upregulated and 1279 downregulated) that were differentially expressed between the cartilage-subchondral bone damage group and the control group. Furthermore, 57 genes were differentially expressed (45 upregulated and 12 downregulated) between the cartilage damage group and the control group. EDNRB was identified in both sets of differentially expressed genes and was thus considered a gene specifically regulated by TXA. Upregulation of EDNRB mRNA in the TXA injection model was confirmed by RT‒qPCR. Notably, immunohistochemistry analysis revealed that EDNRB is involved in PTOA pathogenesis. Conclusion These study results suggest that the ETB receptor plays a pivotal role in cartilage degeneration after acute injury induced by topical administration of TXA and may be a new target for the development of therapies for this condition.