O2 Muu julkaisu
The effect of mannan-binding lectin variant alleles on coronary artery reactivity in healthy young men
Tekijät: Aittoniemi J, Fan YM, Laaksonen R, Janatuinen T, Vesalainer R, Nuutila P, Knuuti J, Hulkkonen J, Hurme M, Lehtimaki T
Kustantaja: ELSEVIER SCI IRELAND LTD
Julkaisuvuosi: 2004
Tietokannassa oleva lehden nimi: INTERNATIONAL JOURNAL OF CARDIOLOGY
Lehden akronyymi: INT J CARDIOL
Vuosikerta: 97
Numero: 2
Aloitussivu: 317
Lopetussivu: 318
Sivujen määrä: 2
ISSN: 0167-5273
DOI: https://doi.org/10.1016/j.ijcard.2003.06.027
Tiivistelmä
Mannan-binding lectin (MBL) is a serum acute-phase protein and a complement component secreted by the liver. Its deficiency caused by point mutations in the MBL gene has recently been associated with severe atherosclerosis. In this study, we investigated the effect of MBL variant alleles on coronary artery reactivity, which is an early marker of coronary dysfunction and predicts the development of atherosclerosis and coronary artery disease. The study population consisted of 51 apparently healthy, normo- or mildly hypercholesterolemic young m en. Myocardial blood flow was measured at baseline and during adenosine-induced hyperemia with positron emission tomography (PET), and MBL genotyping was performed using restriction fragment-length polymorphism. As a result, MBL variant alleles had no effect on coronary artery reactivity. This finding suggests that MBL deficiency is not an independent risk factor for coronary dysfunction and early atherogenic changes but rather a co-factor in the development of atherosclerosis. Thus, the connection of MBL variant alleles with environmental risk factors in atherosclerosis should further be assessed. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
Mannan-binding lectin (MBL) is a serum acute-phase protein and a complement component secreted by the liver. Its deficiency caused by point mutations in the MBL gene has recently been associated with severe atherosclerosis. In this study, we investigated the effect of MBL variant alleles on coronary artery reactivity, which is an early marker of coronary dysfunction and predicts the development of atherosclerosis and coronary artery disease. The study population consisted of 51 apparently healthy, normo- or mildly hypercholesterolemic young m en. Myocardial blood flow was measured at baseline and during adenosine-induced hyperemia with positron emission tomography (PET), and MBL genotyping was performed using restriction fragment-length polymorphism. As a result, MBL variant alleles had no effect on coronary artery reactivity. This finding suggests that MBL deficiency is not an independent risk factor for coronary dysfunction and early atherogenic changes but rather a co-factor in the development of atherosclerosis. Thus, the connection of MBL variant alleles with environmental risk factors in atherosclerosis should further be assessed. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
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