RBM39 upregulation promotes ostium re-obstruction after endoscopic endonasal dacryocystorhinostomy (En-DCR)

<h4>Purpose</h4>Chronic dacryocystitis, characterized by epiphora, is primarily treated with dacryocystorhinostomy (DCR), yet postoperative anastomotic re-obstruction remains a significant cause of failure. This study aimed to identify the key molecular mechanisms driving this recurrence.<h4>Methods</h4>Nasal mucosal tissues were collected from 30 post-DCR patients: 15 with re-obstruction (proliferation group) and 15 with successful outcomes (non-proliferation group). Proteomic analysis based on LC-MS/MS was conducted, with differentially expressed proteins (DEPs) defined by a fold change ≥ 1.5 and p < 0.05. Western blot and immunohistochemistry were used for validation and localization. The role of RBM39 in vascular endothelial cell proliferation was assessed via functional experiments, and its associated pathway was analyzed.<h4>Results</h4>Proteomics identified RBM39 as significantly upregulated in re-obstruction tissues, confirmed to be expressed in the vascular endothelium. In vitro, RBM39 overexpression enhanced HMEC-1 proliferation, while its knockdown suppressed it. KEGG pathway analysis suggested the Focal Adhesion pathway may be involved as a potential downstream mechanism.<h4>Conclusion</h4>This study observes that RBM39 is upregulated at the anastomotic site and correlates with enhanced vascular endothelial cell proliferation. The Focal Adhesion pathway may be implicated in this process, suggesting RBM39 as a candidate target for mitigating postoperative ostium re-obstruction after En-DCR. However, further mechanistic studies are needed to establish a direct causal relationship and evaluate its therapeutic potential.