Association of Primary Varicose Veins with Dysregulated Vein Wall Apoptosis

Ducasse, Éric; Giannakakis, K.; Speziale, Francesco; Midy, D.; Sbarigia, Enrico; Jc, Baste; Faraggiana, Tullio

doi:10.1016/j.ejvs.2007.08.015

Cited by 25 publications

(18 citation statements)

References 26 publications

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“…Nevertheless, dysregulated apoptosis in the walls of varicose veins is attributed to the pathogenesis of the disease [1]. If Bujan and co-authors [13] have found an increase of apoptotic SMCs in the varicose vein wall, then others [10–12, 14] have reported a reduced number of apoptotic cells in varicose veins. Our preliminary data also allow us to speculate that the apoptosis of SMCs in non-varicose veins is higher than that in varicose veins, while in the case of apoptotic ECs the situation is likely the opposite; that is, apoptosis of ECs in nonvaricose veins may be lower.…”

Section: Discussionmentioning

confidence: 99%

“…Both Ducasse with co-authors [10] and Lee with co-authors [8] have reported the downregulation of proapoptotic proteins Bax or Bcl-2 and caspase 9 in the walls of varicose veins showing the involvement of the intrinsic pathway, while no changes were detected in Fas and caspase 8 characterizing the extrinsic signaling pathway. Also Ascher and co-authors [12] have shown that the entry of SMCs into the apoptotic pathway is regulated by Bax, which is downregulated in varicose veins in comparison with healthy veins.…”

Section: Discussionmentioning

confidence: 99%

“…Concerning the role of SMC apoptosis in varicose veins, controversial data have been obtained. Several authors [10–12] have reported reduction of the number of apoptotic SMCs in varicose veins compared with nonvaricose veins. Contrariwise, Bujan and co-authors [13] have found an increase of apoptotic SMCs in varicose veins.…”

Section: Introductionmentioning

confidence: 99%

“…Ducasse and coauthors [10] have immunohistochemically quantified fewer Bax, and caspase-9-positive cells in the wall of varicose veins compared to healthy veins, but no changes were detected in Fas and caspase 8 immunoreactivity. Lee with co-authors [8, 19] have found dysregulation of apoptosis through the intrinsic pathway in the varicose veins and in the internal spermatic veins of patients with varicosele, which allows the authors to speculate that the mechanism of reduced apoptosis might contribute to the dilated and thickened walls of both venous diseases.…”

Section: Introductionmentioning

confidence: 99%

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Associations of NF-kappaB and Bax with Apoptosis in Varicose Veins of Women of Different Age Groups

Simovart

Arend²,

Lieberg³

et al. 2011

International Journal of Vascular Medicine

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The study aimed at detecting apoptotic endothelial cells (ECs) and smooth muscle cells (SMCs) together with determining expression of NF-kappaB (p105/p50) and Bax in varicose vein walls. Women (n = 35) undergoing the excision of varicose veins were divided into 3 groups: younger than 35 years (I), 36–50 years (II), and older than 50 years (III). Apoptosis was determined by the TUNEL method, NF-kappaB and Bax expression by immunohistochemistry. The percentage of apoptotic ECs and SMCs in the layers of varicose vein wall increased in groups II and III. NF-kappaB expression had the lowest level in Group II with particularly low level in the media. Contrariwise, Bax expression levels in Group II were increased. The study revealed that in varicose veins ECs and SMCs apoptosis increased with advancing age. If increase in apoptosis during earlier stages of varicosities is probably regulated by intrinsic pathway, then in older patients other signaling pathways may be involved.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Associations of NF-kappaB and Bax with Apoptosis in Varicose Veins of Women of Different Age Groups

Simovart

Arend²,

Lieberg³

et al. 2011

International Journal of Vascular Medicine

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“…Abnormalities in the apoptotic cell death control contribute to a variety of cardiovascular diseases such as atherosclerosis, aneurysm formation, ischemic cardiomyopathies, infarction, and varicose veins (8-10). Several studies have dealt with apoptosis in the varicose veins of the lower extremities (11,12), but there has been no research on the upper extremities veins.…”

mentioning

confidence: 99%

Assessment of apoptosis in the native vein used for hemodialysis access

et al. 2016

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AimTo determine whether apoptosis is more common in previously punctured native veins than in non-punctured native veins among patients who undergo surgical creation of arteriovenous fistula (AVF) for dialysis access.MethodsCephalic vein specimens were obtained from January 1, 2013 to December 31, 2014 from 60 patients, 30 with previously punctured native veins and 30 with non-punctured native veins. Before AVF placement, a 1-cm vein segment was excised from distal part of the vein for histological, histochemical, and immunohistochemical analysis. Vein specimens were divided into two portions along the longitudinal axis and stained with hematoxylin and eosin for routine histological evaluation. Immunohistochemical analysis was used to localize Bax, p53, caspase 3, and Bcl-2 expression.ResultsThe group with previously punctured veins showed significantly increased caspase 3 (P < 0.001, two-sided Fisher`s Exact Test) and Bax expression (P = 0.002, two-sided Fisher`s Exact Test) and significantly decreased Bcl-2 expression (P < 0.001, two-sided Fisher`s Exact Test) compared with the control group. There were no significant differences between the groups in p53 expression (χ2 = 0.071, df = 1, P = 0.791). Fistula failure was significantly more common in the study group (26.7% vs 6.7%, χ2 = 4.32, df = 1, P = 0.038).ConclusionOur study indicates a possible role of venipuncture in apoptosis development and a possible role of apoptosis in fistula failure, but we do not have sufficient evidence to conclude that it represents its main cause.

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Molecular Genetics of Primary Varicose Vein Disease

Adesina‐Georgiadis

Anwar

Davies

2013

Encyclopedia of Life Sciences

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There is sufficient empirical evidence to suggest that there is a significant genetic contribution to the development of varicose vein (VV) disease. However, it is also clear that VV is a complex disease, which is ultimately determined by a number of genetic and environmental factors. The fact that VV are also a secondary manifestation of other vascular conditions further convolutes the understanding of the aetiology and the underlying molecular mechanisms. Despite there being many techniques which are routinely used to characterise the genetic factors involved, these strategies have inherent limitations. Furthermore, the elucidation of a factor's contribution is a complex process, due to the fact that any effect present may be confounded by other parallel effects. To fully understand the genetic contribution to VV disease, there is a need to formulate a rigorous research protocol which should utilise some of the very advanced genetic approaches. Key Concepts: Family history, age, sex and pregnancy are the established risk factors for varicose vein disease; however, not all individuals with these risk factors develop the disease. Abnormal changes in varicose vein walls have been noticed independent of valve damage suggesting that primary vein wall damage is an epiphenomenon of the disease. However, the molecular mechanism behind the vein wall damage is poorly understood. Empirical evidence suggests a strong genetic link to the disease; however, questionnaire‐based studies are subject to biases. There are several approaches available to determine the genetic link. Genes expression profiling using microarray technique has been used in varicose veins but it does not explain whether the expressed genes are the cause or the effect of the disease. Candidate gene studies have shown that FOXC2, desmuslin, thrombomodulin and methylenetetrahydrofolate reductase have been found to be associated with varicose veins. Candidate gene approach requires a very detailed knowledge of the disease biology which unfortunately does not exist for varicose veins. Synchronised use of technologies including genome‐wide association study (GWAS), metabonomics and micro‐RNA analysis have the potential to elucidate the molecular mechanism of the disease and identify the underlying genetic association.

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Association of Primary Varicose Veins with Dysregulated Vein Wall Apoptosis

Abstract: Apoptosis is down regulated in the medial layer of varicose veins. This dysregulation is attributable to a disorder of the intrinsic pathway and involves the great saphenous vein trunk, major tributaries and accessory veins. This process may be among the causes of primary varicose veins.

Cited by 25 publications

References 26 publications

Associations of NF-kappaB and Bax with Apoptosis in Varicose Veins of Women of Different Age Groups

Associations of NF-kappaB and Bax with Apoptosis in Varicose Veins of Women of Different Age Groups

Assessment of apoptosis in the native vein used for hemodialysis access

Molecular Genetics of Primary Varicose Vein Disease

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