Transforming growth factor (TGF)‐β 1 inversely related to vascular cell adhesion molecule‐1 in postmenopausal women with coronary artery disease. A possible mechanism for the putative cardioprotective role of TGF‐β 1 ?
Os I, Djurovic S, Seljeflot I, Berg K (Ullevål University Hospital, Oslo, Norway). Transforming growth factor (TGF)‐β 1 inversely related to vascular cell adhesion molecule‐1 in postmenopausal women with coronary artery disease. A possible mechanism for the putative cardioprotective role of TGF‐β 1...
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Published in | Journal of internal medicine Vol. 251; no. 3; pp. 223 - 227 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
03.03.2002
|
Online Access | Get full text |
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Summary: | Os I, Djurovic S, Seljeflot I, Berg K (Ullevål University Hospital, Oslo, Norway). Transforming growth factor (TGF)‐β
1
inversely related to vascular cell adhesion molecule‐1 in postmenopausal women with coronary artery disease. A possible mechanism for the putative cardioprotective role of TGF‐β
1
?
J Intern Med
2002;
251:
223–227.
Objective and design.
Transforming growth factor beta (TGF‐β
1
) is involved in a variety of physiological processes as well as in many diseases. Both
in vitro
and
in vivo
evidence suggest that TGF‐β
1
may influence atherogenesis and a dominant protective role of TGF‐β
1
on coronary arteries has been proposed. On the other hand, increased levels of soluble adhesion molecules have been found in patients with atherosclerosis, and adhesion of monocytes to the endothelium followed by migration to the intima, has been proved to be an early event in atherosclerosis. The purpose of the present investigation was to look at a possible relationship between circulating active TGF‐β
1
and adhesion molecules in postmenopausal women with angiographically verified coronary heart disease (CHD) (
n
=118).
Results.
Serum levels of the active form of TGF‐β
1
showed a tendency to be lower in patients with increasing number of vessels with more than 50% stenosis (
P
=0.058), and there was higher TGF‐β
1
in the group with one vessel disease compared with those with two or more vessels affected (
P
=0.041). Additionally, negative association between TGF‐β
1
and VCAM‐1 was found (
r
=–0.26,
P
=0.023). However, no associations were observed between TGF‐β
1
and intercellular adhesion molecule‐1 (ICAM‐1) or E‐selectin in the present study.
Conclusion.
We observed an inverse correlation between the active form of TGF‐β
1
and VCAM‐1 in postmenopausal women with verified CHD. These results may suggest a role of TGF‐β
1
in CHD. |
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ISSN: | 0954-6820 1365-2796 |
DOI: | 10.1046/j.1365-2796.2002.00950.x |