Sapheno-Femoral Junction Pathology: Molecular Mechanism of Saphenous Vein Incompetence

A molecular mechanism responsible for varicose vein occurrence was investigated. The role of potential cell cycle regulator p21 and programmed cell death in the pathology leading to the proximal long saphenous vein (LSV) incompetence was investigated. Proximal LSV specimens were obtained from 40 pat...

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Bibliographic Details
Published in:Clinical and applied thrombosis/hemostasis 2004-10, Vol.10 (4), p.311-321
Main Authors: Urbanek, Tomasz, Skop, Barbara, Ziaja, Krzysztof, Wilczok, Tadeusz, Wiaderkiewicz, Ryszard, Pal/asz, Artur, Mazurek, Urszula, Wielgus, Ewa
Format: Article
Language:English
Subjects:
Adult
Aged
Apoptosis
Case-Control Studies
Cell cycle
Cell Cycle Proteins - analysis
Cell Cycle Proteins - genetics
Cyclin-Dependent Kinase Inhibitor p21
fas Receptor - analysis
fas Receptor - genetics
Female
Humans
Immunohistochemistry
Male
Middle Aged
Muscle, Smooth, Vascular - pathology
Proliferating Cell Nuclear Antigen - analysis
Proliferating Cell Nuclear Antigen - genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - analysis
Saphenous Vein - chemistry
Saphenous Vein - pathology
Tissue Distribution
Tumor Suppressor Protein p53 - analysis
Tumor Suppressor Protein p53 - genetics
Varicose Veins - etiology
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Summary:A molecular mechanism responsible for varicose vein occurrence was investigated. The role of potential cell cycle regulator p21 and programmed cell death in the pathology leading to the proximal long saphenous vein (LSV) incompetence was investigated. Proximal LSV specimens were obtained from 40 patients with primary varicose veins who had undergone crossectomy. The expression of the p21, p53, and fas encoding genes was investigated by the means of real-time RT-QPCR. Immunostaining for gene product presence, proliferating cell nuclear antigen (PCNA), and apoptotic cells (TUNEL assay) was carried out. The results were compared to the control healthy vein specimens and correlated with pathologic examination findings (of the valve and vein structure). A significant increase in p21, p53, and fas mRNA expression were reported in the proximal incompetent veins. The expression of p21 correlated with expression of p53 (r = 0.658; p
ISSN:1076-0296
1938-2723
DOI:10.1177/107602960401000403