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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Published in: | Clinical and applied thrombosis/hemostasis Vol. 10; no. 4; p. 311 |
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01-10-2004
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Abstract | 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<0.05) and negative correlation between media apoptotic index and p21 mRNA expression was found (r = -0.493; p<0.05). Decrease in the muscular component within the media and disturbances of the local structure in the incompetent LSVs were reported. Fas overexpression did not correlate with p53 expression level and did not correlate with apoptotic cell number in the respective vein layers. PCNA-positive cells were present more frequently in the media of the control veins, especially in young subjects. Apoptosis downregulation, cell cycle inhibition and smooth muscle cell hypertrophy are important factors influencing vein wall disturbances related to sapheno-femoral junction incompetence. |
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AbstractList | 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<0.05) and negative correlation between media apoptotic index and p21 mRNA expression was found (r = -0.493; p<0.05). Decrease in the muscular component within the media and disturbances of the local structure in the incompetent LSVs were reported. Fas overexpression did not correlate with p53 expression level and did not correlate with apoptotic cell number in the respective vein layers. PCNA-positive cells were present more frequently in the media of the control veins, especially in young subjects. Apoptosis downregulation, cell cycle inhibition and smooth muscle cell hypertrophy are important factors influencing vein wall disturbances related to sapheno-femoral junction incompetence. |
Author | Skop, Barbara Wilczok, Tadeusz Ziaja, Krzysztof Urbanek, Tomasz Pałasz, Artur Mazurek, Urszula Wiaderkiewicz, Ryszard Wielgus, Ewa |
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CitedBy_id | crossref_primary_10_1177_00033197241256680 crossref_primary_10_1177_17085381211012882 crossref_primary_10_1016_j_jvsv_2024_101941 crossref_primary_10_1177_0268355515580474 |
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Snippet | A molecular mechanism responsible for varicose vein occurrence was investigated. The role of potential cell cycle regulator p21 and programmed cell death in... |
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SubjectTerms | Adult Aged Apoptosis Case-Control Studies 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 |
Title | Sapheno-femoral junction pathology: molecular mechanism of saphenous vein incompetence |
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