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Retinoids and fibrinolysis
1Department of Dermatology, University Hospital, Umeå, Sweden.
Acta Dermato-Venereologica
|July 1, 1995
Summary
Retinoids, like retinoic acid, enhance tissue plasminogen activator (t-PA) release from endothelial cells without increasing plasminogen activator inhibitor-1 (PAI-1). This suggests a safer profile for long-term dermatological retinoid therapy regarding cardiovascular risk.
Area of Science:
- Biochemistry
- Dermatology
- Cardiovascular Research
Background:
- Vitamin A analogues, or retinoids, have shown potential to increase tissue plasminogen activator (t-PA) release in laboratory settings.
- Dermatological therapies often utilize retinoids, necessitating an understanding of their impact on fibrinolytic factors.
Purpose of the Study:
- To reevaluate the in vitro effects of retinoids on endothelial fibrinolytic factors.
- To investigate if therapeutic doses of retinoids enhance endothelial fibrinolytic factor release.
- To assess the safety implications of retinoid therapy on cardiovascular health.
Main Methods:
- In vitro incubation of endothelial cells with retinoic acid.
- Analysis of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in cell supernatant.
- Plasma analysis of t-PA, PAI-1, and von Willebrand factor in patients treated with isotretinoin or etretinate.
Main Results:
- Retinoic acid significantly increased t-PA release from endothelial cells in vitro.
- No concurrent increase in PAI-1 secretion was observed with retinoic acid treatment.
- Patients on isotretinoin or etretinate showed elevated baseline t-PA plasma levels.
- PAI-1 and von Willebrand factor levels remained unchanged in patients undergoing retinoid therapy.
Conclusions:
- Therapeutic doses of retinoids promote chronic augmentation of t-PA secretion.
- Evidence suggests no endothelial cell damage associated with this enhanced t-PA release.
- Findings may influence the interpretation of long-term retinoid therapy safety, particularly concerning cardiovascular risks linked to hyperlipemia.