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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Wolanska M. 1, Bankowska-Guszczyn E. 1, Sobolewski K. 1, Kowalewski R. 2
1 Department of Medical Biochemistry; Medical University of Bialystok, Bialystok, Poland;
2 Department of Vascular Surgery and Transplantology, Medical University of Bialystok, Bialystok, Poland
AIM: The development of abdominal aortic aneurysm (AAA) is thought to be related to an imbalance of VEGF and its receptors. This study aimed at evaluating the expression of VEGF family members and their receptors in AAA wall, AAA mural thrombus and normal aorta wall.
METHODS: AAA specimens (mural thrombus-luminal layer, mural thrombus-abluminal layer, AAA wall) were collected from 24 patients undergoing elective open AAA repair. Abdominal aortas from 12 organ donors served as controls. The expression of VEGF (VEGF-A, VEGF-B, VEGF-C and VEGF-D) and VEGF receptors (VEGFR-1, VEGFR-2 and VEGFR-3) was evaluated using Western blot.
RESULTS: Increased expression of VEGF-B (269±31%), VEGF-C (1065±92%) and VEGF-D (145±12%) was found in AAA wall, when compared to normal aorta (P<0.01). No significant difference in VEGF-A expression was demonstrated between AAA and normal aortic wall (P>0.01). Mural thrombus (abluminal/luminal) expression of VEGF-A (172±22%/133±17%), VEGF-B (308±24% / 363±28%), VEGF-C (1496±110%/830±58%) and VEGF-D (200±18%/142±12%) was increased in comparison with normal aorta (P<0.01). Furthermore, VEGF-C and VEGF-D expression was increased in mural thrombus abluminal layer, when compared to its luminal layer (1496±110% vs. 830±58% and 200±18% vs. 142±12%, P<0.01). VEGFR-1 expression was increased only in luminal and abluminal layers of mural thrombus (377±58% and 2188±196%, P<0.01). In comparison with normal aorta, all aneurysm samples (AAA wall, mural thrombus abluminal and luminal layers) expressed higher levels of VEGFR-2 (565±52%, 1057±125%, 537±54%, P<0.01) and VEGFR-3 (233±18%, 197±17%, 193±16%, P<0.01).
CONCLUSIONS: Our study demonstrates that the abluminal layer in AAA mural thrombus contains high levels of VEGFs and VEGF receptors, suggesting that this layer may play a significant role in AAA disease pathogenesis. Increased expressions of VEGF and their receptors in AAA mural thrombus may impact different pathways involved in AAA etiology.