Background: Implantation of a retrievable vena cava filter (VCF) is an effective method for preventing pulmonary embolism. Retrieval of filters, however, may be difficult due to intimal hyperplasia and inflammation in the cava wall. The transcription factor nuclear factor-kappaB (NF-κB) plays an important role in regulation of numerous genes participating in the inflammatory and proliferative responses of cells. The present study was to determine whether VCF implantation resulted in activation of NF-κB in the venous neointima.
Methods: Filters were placed in vena cava (VC) in four swine for 30 days and then removed. Intimal specimens adhering to the filter struts were analyzed with reference to normal VC tissues. Immunohistochemical analyses were used to assess the NF-κB subunits p65 and p50 and the phosphorylated inhibitor of κB-α (phosphor-IκB-α) in the tissues. NF-κB DNA-binding activity was measured with enzyme-linked immunosorbent assay.
Results: As compared to normal VC tissues, the intimal tissues contained higher percentages of cell nucleus-located p65 and p50, and NF-κB DNA-binding activity. Elevated immunoreactivities of p65, p50 and phosphor-IκB-α were also present in the intima.
Conclusion: The present study demonstrates for the first time that VCF implantation caused NF-κB activation in neointima. We further demonstrate the activation is at least partly due to phosphorylation of IκB-α. Our data suggest that NF-κB activation would significantly contribute to development of intimal hyperplasia and inflammation in filter-inserted vena cava walls. NF-κB might be a therapeutic target for inhibiting filter-induced neointima and improving filter retrieval.
Keywords: Intima; IκB-α; NF-κB; Vena cava filter.