The inflammatory reaction during chronic venous disease of lower limbs.

Ojdana, Dominika; Safiejko, Kamil; Lipska, Alina; Sacha, Paweł; Wieczorek, Piotr; Radziwon, Piotr; Dadan, Jacek; Tryniszewska, Elżbieta

doi:10.2478/v10042-009-0029-8

Cited by 15 publications

(11 citation statements)

References 40 publications

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“…Our data confirm the validity of the many authors point of view (3,(5)(6)(7)(8)(9), that the basis of superficial veins varicose transformation and development of their valves insufficiency is an inflammatory process. At the same time, our results revealed another important pattern, which previously has not been described in the literature.…”

Section: Discussionsupporting

confidence: 91%

“…Recent data indicate that the inflammatory process causes the structural readjustment of the veins wall and venous valves (3,(5)(6)(7)(8)(9). This is confirmed through infiltration of the venous wall and valve flappers by monocytes and macrophages.…”

Section: Vitebsk State Medical University Republic Of Belarusmentioning

confidence: 88%

“…Moreover, cell infiltrates appear in the venous wall zones, endotheliocytes of which produce the endothelial cell adhesion mole cules (1,5,(10)(11)(12). Proteolytic enzymes, in particular, matrix metalloproteinases synthesized by macrophages and endothelial cells, cause degradation of the proteins forming the extracellular matrix of the vein wall (5,8,9,(11)(12)(13)(14)(15). Thus, a cascade of inflammatory changes accompanied by discharging of inflammatory mediators and growth factors, leads to the transformation and destruction of the valves (2,6,8,11).…”

Section: Vitebsk State Medical University Republic Of Belarusmentioning

confidence: 99%

See 2 more Smart Citations

Expression of the proinflammatory marker CD34 in varicose leg veins

Sushkou¹,

Samsonava²,

Galishevich³

2015

Phlebologie

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Section: Discussionsupporting

confidence: 91%

Section: Vitebsk State Medical University Republic Of Belarusmentioning

confidence: 88%

Section: Vitebsk State Medical University Republic Of Belarusmentioning

confidence: 99%

See 1 more Smart Citation

Expression of the proinflammatory marker CD34 in varicose leg veins

Sushkou¹,

Samsonava²,

Galishevich³

2015

Phlebologie

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show abstract

“…That may explain increased TGF-β1 activation in the course of thrombophlebitis. But on the other hand, TGF-β1 induces MMP-9 activation [33,34]. Thus, it still needs to be clarified if enhanced TGF-β1 activation results from increased MMP-9 activity or leads to increased MMP-9 activation.…”

Section: Discussionmentioning

confidence: 99%

Influence of thrombophlebitis on TGF-Î˛1 and its signaling pathway in the vein wall.

Kowalewski

Małkowski²,

Gacko³

et al. 2011

Folia Histochem Cytobiol.

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Extensive extracellular matrix remodeling of the vein wall is involved in varicose veins pathogenesis. This process is controlled by numerous factors, including peptide growth factors. The aim of the study was to evaluate influence of thrombophlebitis on TGF-β1 and its signaling pathway in the vein wall. TGF-β1 mRNA levels, growth factor content and its expression were evaluated by RT-PCR, ELISA, and western blot methods, respectively, in the walls of normal veins, varicose veins and varicose veins complicated by thrombophlebitis. Western blot analysis was used to assess TGF-β receptor type II (TGF-β RII) and p-Smad2/3 protein expression in the investigated material. Unchanged mRNA levels of TGF-β1, decreased TGF-β1 content, as well as decreased expression of latent and active forms of TGF-β1 were found in varicose veins. Increased expression of TGF-β RII and p-Smad2/3 were found in varicose veins. Thrombophlebitis led to increased protein expression of the TGF-β1 active form and p-Smad2/3 in the vein wall compared to varicose veins. TGF-β1 may play a role in the disease pathogenesis because of increased expression and activation of its receptor in the wall of varicose veins. Thrombophlebitis accelerates activation of TGF-β1 and activity of its receptor in the varicose vein wall.

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“…The reason of the majority of CVD symptoms, (teleangiectases, varicose veins, edema, trophic changes, chronic leg ulceration), is prolonged venous hypertension caused by venous wall abnormalities and venous valves incompetence [30]. Recent advantages in understanding of CVD are focused on role of the leukocytes in the CVD pathogenesis [31].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the memory CD4+ and CD8+ T cells homeostasis during chronic venous disease of lower limbs.

Ojdana

Safiejko²,

Milewski³

et al. 2010

Folia Histochem Cytobiol.

Self Cite

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More and more is known about the role of venous wall abnormalities and valvular incompetence in the development of chronic venous disorders (CVD). Unfortunately detailed mechanisms of CVD pathophysiology are not well understood. Recent studies focus on involvement of the inflammatory process in the structural remodeling of venous valvues and venous wall. The aim of this study is to investigate and to document the memory T cells homeostasis in CVD patients. In this study we present lymphocytic changes in blood from varicose veins in terms of total CD4+ and CD8+ T cells and their particular subsets of memory T cells: T N , T CM and T EM . Results suggest that immunological memory may be involved in the CVD development.

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The inflammatory reaction during chronic venous disease of lower limbs.

Cited by 15 publications

References 40 publications

Expression of the proinflammatory marker CD34 in varicose leg veins

Expression of the proinflammatory marker CD34 in varicose leg veins

Influence of thrombophlebitis on TGF-Î˛1 and its signaling pathway in the vein wall.

Evaluation of the memory CD4+ and CD8+ T cells homeostasis during chronic venous disease of lower limbs.

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