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Atorvastatin suppresses homocysteine formation in stimulated human peripheral blood mononuclear cells.
Clin Chem Lab Med. 2005; 43(12):1373-6.CC

Abstract

Hyperhomocysteinemia is regarded as an independent risk factor for vascular diseases, and homocysteine is supposed to contribute to oxidative stress and endothelial damage. Statin therapy is an established intervention to reduce the risk of acute events in patients suffering from cardiovascular diseases. Apart from their lipid-lowering capacity, statins also exert anti-inflammatory and antioxidant effects. As cellular immune activation and oxidative stress play a major role in the pathogenesis of cardiovascular diseases, the anti-inflammatory capacity of statins could partly be responsible for the beneficial effects observed in patients. Earlier we reported that stimulated peripheral blood mononuclear cells (PBMCs) release homocysteine. Here we studied the influence of atorvastatin on homocysteine production in stimulated PBMCs and compared changes in cysteine concentrations and in neopterin production, which is a sensitive indicator of cellular immune activation. Stimulation of human PBMCs with the mitogens concanavalin A and phytohemagglutinin induced significant homocysteine and neopterin production compared to unstimulated cells, whereas cysteine concentrations remained unchanged. Treatment of PBMCs with increasing doses of atorvastatin (10-100 microM) suppressed both biochemical pathways in a dose-dependent manner, and cell proliferation was inhibited in parallel. Again, cysteine levels were not influenced by any treatment. The down-regulating effect of atorvastatin on homocysteine formation in vitro indicates that statins may prevent homocysteine accumulation in the blood via immunosuppression.

Authors+Show Affiliations

Division of Biological Chemistry, Biocenter, Innsbruck Medical University, and Ludwig Boltzmann Institute of AIDS Research, Innsbruck, Austria.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16309375

Citation

Schroecksnadel, Katharina, et al. "Atorvastatin Suppresses Homocysteine Formation in Stimulated Human Peripheral Blood Mononuclear Cells." Clinical Chemistry and Laboratory Medicine, vol. 43, no. 12, 2005, pp. 1373-6.
Schroecksnadel K, Frick B, Winkler C, et al. Atorvastatin suppresses homocysteine formation in stimulated human peripheral blood mononuclear cells. Clin Chem Lab Med. 2005;43(12):1373-6.
Schroecksnadel, K., Frick, B., Winkler, C., Wirleitner, B., Weiss, G., & Fuchs, D. (2005). Atorvastatin suppresses homocysteine formation in stimulated human peripheral blood mononuclear cells. Clinical Chemistry and Laboratory Medicine, 43(12), 1373-6.
Schroecksnadel K, et al. Atorvastatin Suppresses Homocysteine Formation in Stimulated Human Peripheral Blood Mononuclear Cells. Clin Chem Lab Med. 2005;43(12):1373-6. PubMed PMID: 16309375.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Atorvastatin suppresses homocysteine formation in stimulated human peripheral blood mononuclear cells. AU - Schroecksnadel,Katharina, AU - Frick,Barbara, AU - Winkler,Christiana, AU - Wirleitner,Barbara, AU - Weiss,Günter, AU - Fuchs,Dietmar, PY - 2005/11/29/pubmed PY - 2006/3/10/medline PY - 2005/11/29/entrez SP - 1373 EP - 6 JF - Clinical chemistry and laboratory medicine JO - Clin. Chem. Lab. Med. VL - 43 IS - 12 N2 - Hyperhomocysteinemia is regarded as an independent risk factor for vascular diseases, and homocysteine is supposed to contribute to oxidative stress and endothelial damage. Statin therapy is an established intervention to reduce the risk of acute events in patients suffering from cardiovascular diseases. Apart from their lipid-lowering capacity, statins also exert anti-inflammatory and antioxidant effects. As cellular immune activation and oxidative stress play a major role in the pathogenesis of cardiovascular diseases, the anti-inflammatory capacity of statins could partly be responsible for the beneficial effects observed in patients. Earlier we reported that stimulated peripheral blood mononuclear cells (PBMCs) release homocysteine. Here we studied the influence of atorvastatin on homocysteine production in stimulated PBMCs and compared changes in cysteine concentrations and in neopterin production, which is a sensitive indicator of cellular immune activation. Stimulation of human PBMCs with the mitogens concanavalin A and phytohemagglutinin induced significant homocysteine and neopterin production compared to unstimulated cells, whereas cysteine concentrations remained unchanged. Treatment of PBMCs with increasing doses of atorvastatin (10-100 microM) suppressed both biochemical pathways in a dose-dependent manner, and cell proliferation was inhibited in parallel. Again, cysteine levels were not influenced by any treatment. The down-regulating effect of atorvastatin on homocysteine formation in vitro indicates that statins may prevent homocysteine accumulation in the blood via immunosuppression. SN - 1434-6621 UR - https://www.unboundmedicine.com/medline/citation/16309375/Atorvastatin_suppresses_homocysteine_formation_in_stimulated_human_peripheral_blood_mononuclear_cells_ L2 - https://www.degruyter.com/doi/10.1515/CCLM.2005.234 DB - PRIME DP - Unbound Medicine ER -