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Modulation of urokinase-type and tissue-type plasminogen activator occurs at an early stage of progressing stages of chronic venous insufficiency.
Acta Derm Venereol. 2000 May; 80(3):162-6.AD

Abstract

Chronic venous insufficiency (CVI) progresses through a series of clinical stages, from healthy skin to poorly healing leg ulcers. The aim of this study was to analyse the distribution pattern and activity level of urokinase-type (uPA) and tissue-type plasminogen activators (tPA) in normal skin and in tissue biopsies of progressing stages of CVI, prior to and including venous ulceration. Biopsies 6 mm thick were taken from 14 healthy volunteers and 37 patients with 5 different stages of CVI: telangiectases; stasis dermatitis; hyperpigmentation; lipodermatosclerosis; and leg ulcer. Changes in the enzymatic activity and spatial localization of uPA and tPA during the progression of CVI were examined using in situ histological zymography. Normal skin and skin with telangiectases showed a punctate PA activity, consisting of both uPA and tPA activity. As CVI progressed, an increase in the distribution of uPA and a decrease in tPA activity was observed. The spatial localization of uPA was widespread within the dermis of biopsies from stasis dermatitis and lipodermatosclerosis and was associated in particular with the dermoepidermal junction. Hyperpigmented skin revealed a pattern of PA expression similar to that of healthy skin. However, leg ulcer specimens exhibited peak levels of uPA with little tPA. Furthermore, a plasminogen-independent protease activity that was not present in any of the earlier stages of CVI appeared. Our results indicate that there are profound changes in PA activity during the progression of CVI and that these changes begin early in CVI, for example, in stasis dermatitis. We hypothesize that the balance or imbalance of the PA activity in the later stages of CVI is an important pathogenic factor for the development of venous leg ulcer.

Authors+Show Affiliations

Department of Dermatology, University of Freiburg, Germany. Peschen@haut.ukl.uni-freiburg.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10954203

Citation

Peschen, M, et al. "Modulation of Urokinase-type and Tissue-type Plasminogen Activator Occurs at an Early Stage of Progressing Stages of Chronic Venous Insufficiency." Acta Dermato-venereologica, vol. 80, no. 3, 2000, pp. 162-6.
Peschen M, Rogers AA, Chen WY, et al. Modulation of urokinase-type and tissue-type plasminogen activator occurs at an early stage of progressing stages of chronic venous insufficiency. Acta Derm Venereol. 2000;80(3):162-6.
Peschen, M., Rogers, A. A., Chen, W. Y., & Vanscheidt, W. (2000). Modulation of urokinase-type and tissue-type plasminogen activator occurs at an early stage of progressing stages of chronic venous insufficiency. Acta Dermato-venereologica, 80(3), 162-6.
Peschen M, et al. Modulation of Urokinase-type and Tissue-type Plasminogen Activator Occurs at an Early Stage of Progressing Stages of Chronic Venous Insufficiency. Acta Derm Venereol. 2000;80(3):162-6. PubMed PMID: 10954203.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of urokinase-type and tissue-type plasminogen activator occurs at an early stage of progressing stages of chronic venous insufficiency. AU - Peschen,M, AU - Rogers,A A, AU - Chen,W Y, AU - Vanscheidt,W, PY - 2000/8/23/pubmed PY - 2001/2/28/medline PY - 2000/8/23/entrez SP - 162 EP - 6 JF - Acta dermato-venereologica JO - Acta Derm Venereol VL - 80 IS - 3 N2 - Chronic venous insufficiency (CVI) progresses through a series of clinical stages, from healthy skin to poorly healing leg ulcers. The aim of this study was to analyse the distribution pattern and activity level of urokinase-type (uPA) and tissue-type plasminogen activators (tPA) in normal skin and in tissue biopsies of progressing stages of CVI, prior to and including venous ulceration. Biopsies 6 mm thick were taken from 14 healthy volunteers and 37 patients with 5 different stages of CVI: telangiectases; stasis dermatitis; hyperpigmentation; lipodermatosclerosis; and leg ulcer. Changes in the enzymatic activity and spatial localization of uPA and tPA during the progression of CVI were examined using in situ histological zymography. Normal skin and skin with telangiectases showed a punctate PA activity, consisting of both uPA and tPA activity. As CVI progressed, an increase in the distribution of uPA and a decrease in tPA activity was observed. The spatial localization of uPA was widespread within the dermis of biopsies from stasis dermatitis and lipodermatosclerosis and was associated in particular with the dermoepidermal junction. Hyperpigmented skin revealed a pattern of PA expression similar to that of healthy skin. However, leg ulcer specimens exhibited peak levels of uPA with little tPA. Furthermore, a plasminogen-independent protease activity that was not present in any of the earlier stages of CVI appeared. Our results indicate that there are profound changes in PA activity during the progression of CVI and that these changes begin early in CVI, for example, in stasis dermatitis. We hypothesize that the balance or imbalance of the PA activity in the later stages of CVI is an important pathogenic factor for the development of venous leg ulcer. SN - 0001-5555 UR - https://www.unboundmedicine.com/medline/citation/10954203/Modulation_of_urokinase_type_and_tissue_type_plasminogen_activator_occurs_at_an_early_stage_of_progressing_stages_of_chronic_venous_insufficiency_ DB - PRIME DP - Unbound Medicine ER -