Expression of Elastic Components in Healthy and Varicose Veins

Buján, Julia; Gimeno, María José Pena; Jiménez, José Alberto Rojas; Kielty, Cay M.; Mecham, Robert P.; Bellón, Juan M.

doi:10.1007/s00268-003-6897-8

Cited by 34 publications

(35 citation statements)

References 26 publications

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“…Other papers have also suggested a potential role of MMPs in extracellular matrix digestion and reorganization, and some MMPs appear to cause vessel enlargement [9]. In a recent study [10], we found changes in the varicose condition in expression levels of vein elastic components and proteolytic enzymes that would appear to indicate their greater metabolism in affected areas.…”

Section: Introductionmentioning

confidence: 89%

TGF-β<sub>1</sub> Upregulation in the Aging Varicose Vein

Pascual¹,

Mendieta²,

García‐Honduvilla

et al. 2007

J Vasc Res

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Background: Although the etiology of venous insufficiency is not well understood, immune response and aging are beginning to emerge as contributing factors. Factors involved in tissue remodeling such as TGF-β₁ also seem to play an important role in extracellular matrix production. The aim of this study was to explore the relationship between chronic venous insufficiency and TGF-β₁ examining the latent/mature form of TGF-β₁ and the presence of mast cells. Effects of age were also evaluated. Methods: Saphenous veins were obtained from patients subjected to aortocoronary bypass (controls) and undergoing varicose vein surgery. These were immunolabeled using anti-LAP TGF-β₁/anti-TGF-β₁ antibodies and subjected to Western blot. Mast cell population was identified by metachromatic staining.Results:Latent TGF-β₁ was significantly reduced in varicose veins from older subjects. In contrast, smooth muscle cells obtained from the varicosities showed intense levels. Mature TGF-β₁ significantly differed between healthy and varicose veins. No mature TGF-β₁ was detected in the cell cultures. Mast cell number and degranulation were increased with aging and varicose disease, colocalizing with the mature form of TGF-β₁. Conclusion: Aging and varicose pathology induce dysregulation of TGF-β₁ that could play an important role in the fibrous process, representing the final stages of venous insufficiency.

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Section: Introductionmentioning

confidence: 89%

TGF-β<sub>1</sub> Upregulation in the Aging Varicose Vein

Pascual¹,

Mendieta²,

García‐Honduvilla

et al. 2007

J Vasc Res

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“…In the present study we therefore investigated the expression of ER ␤ in relation to apoptosis and cellular hypertrophy of SMC in both varicose and nonvaricose veins by using new stereological tools [16,17] . Since age induces changes in the histological structure of the vein wall [18] and to avoid gender differences, we studied varicose and nonvaricose veins from age-matched male subjects.…”

Section: Introductionmentioning

confidence: 99%

Smooth Muscle Cell Hypertrophy in Varicose Veins Is Associated with Expression of Estrogen Receptor-β

Knaapen¹,

Somers²,

Bortier³

et al. 2005

J Vasc Res

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Varicose veins are characterized by dilated and thickened vein walls. This study examined whether the changes that occur in varicose veins are associated with smooth muscle cell (SMC) hypertrophy, cellular proliferation or apoptosis. Moreover, the association between SMC hypertrophy and the expression of the estrogen receptor-β (ERβ) was investigated. Varicose veins were obtained from male patients during vascular stripping surgery (n = 11) and nonvaricose veins during coronary bypass surgery, also from male subjects (n = 12). The cellular volume of the SMC in both the longitudinal and circular layer of the vessel wall was measured using stereological methods. Apoptosis was detected using the TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling) technique. SMC proliferation and ERβ expression were investigated by immunohistochemistry. Neither in the longitudinal nor in the circular layer of the varicose vein wall were signs of apoptosis or proliferation present. However, the mean cellular volume of the SMC in the circular layer of the varicose veins was strongly increased (5,291 ± 363 µm³) as compared to non-varicose veins (2,812 ± 212 µm³, p < 0.001). Moreover, ERβ expression in the circular layer of varicose veins (63 ± 4%) significantly differed from nonvaricose veins (39 ± 4%; p = 0.001). Interestingly, the SMC volume correlated with ERβ expression (r = 0.71, p < 0.001). These data show that cell death or proliferation of SMC do not, or only rarely, occur in varicose veins. However, remodeling of varicose veins can mainly be attributed to increased volumes of the SMC of the circular layer and this increase correlates with ERβ expression.

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“…The growth factor protein content, as well as protein expression of TGF-␤ 1 latent and active forms, is also increased in varicose veins [7][8][9] . Furthermore, immunohistochemistry revealed increased staining for TGF-␤ 1 in tissue sections, as well as in cell cultures from varicose veins [8,9,16] . However, tissue responsiveness to TGF-␤ 1 depends on numerous factors, including TGF-␤ RII expression and activation [5,12] .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Transforming Growth Factor-β Signaling Pathway in the Wall of Normal and Varicose Veins

Kowalewski

Małkowski²,

Sobolewski³

et al. 2010

Pathobiology

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Objective(s): Extracellular matrix remodeling in the vein wall is involved in varicose vein pathogenesis, with transforming growth factor β₁ (TGF-β₁) playing a potential role. The aim of the study was to assess the TGF-β signaling pathway including its receptor (TGF-β RII) and phosphorylated receptor-regulated Smads (p-Smad2/3) in varicose veins. Methods: Varicose veins from patients undergoing varicose vein surgery were the studied material, whereas normal greater saphenous veins from patients undergoing infrainguinal arterial bypass surgery were the control material. Expression of TGF-β RII mRNA was assessed with RT-PCR, whereas expression of TGF-β RII and p-Smad2/3 proteins was assessed with Western blot. Results: A significantly increased TGF-β RII mRNA level was found in varicose veins (287 ± 24%), when compared with normal veins (100 ± 26%). The receptor protein expression reflected a changed mRNA level with significantly increased TGF-β RII protein in varicose veins (290 ± 21%), when compared with controls (100 ± 16%). Enhanced TGF-β RII expression was accompanied by increased p-Smad2/3 protein expression in varicose veins (257 ± 19%) in comparison with normal veins (100 ± 9%). Conclusion(s): Increased TGF-β RII expression and activation in the wall of varicose veins may be involved in extracellular matrix remodeling related to TGF-β₁ and supports its role in the disease pathogenesis.

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Expression of Elastic Components in Healthy and Varicose Veins

Cited by 34 publications

References 26 publications

TGF-β<sub>1</sub> Upregulation in the Aging Varicose Vein

TGF-β<sub>1</sub> Upregulation in the Aging Varicose Vein

Smooth Muscle Cell Hypertrophy in Varicose Veins Is Associated with Expression of Estrogen Receptor-β

Evaluation of Transforming Growth Factor-β Signaling Pathway in the Wall of Normal and Varicose Veins

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