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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:2776-2782

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:2776-2782.)
© 1997 American Heart Association, Inc.


Articles

Moderate Genetic Influences on Plasma Levels of Plasminogen Activator Inhibitor-1 and Evidence of Genetic and Environmental Influences Shared by Plasminogen Activator Inhibitor-1, Triglycerides, and Body Mass Index

Yuling Hong; Nancy L. Pedersen; Nils Egberg; ; Ulf de Faire

From the Divisions of Cardiovascular and Genetic Epidemiology, Institute of Environmental Medicine, The Karolinska Institute, Stockholm, Sweden (Y.H., N.L.P., U.d.F.); the Division of Cardiovascular Medicine, Department of Medicine (Y.H., U.d.F.) and the Department of Clinical Chemistry (N.E.), Karolinska Hospital, Stockholm, Sweden; and the Center for Development and Health Genetics, College of Health and Human Development, the Pennsylvania State University, University Park, Pa.

Correspondence to Dr Yuling Hong, Divisions of Cardiovascular and Genetic Epidemiology, Institute of Environmental Medicine, Box 210, Doktorsringen 16C, The Karolinska Institute, 171 77 Stockholm, Sweden. E-mail yuling{at}wubios.wustl.edu

Abstract Both genes and environmental factors have been reported to influence plasma levels of plasminogen activator inhibitor-1 (PAI-1). However, the relative importance of genetic influences (ie, heritability) on plasma PAI-1 levels has not yet been investigated. Furthermore, PAI-1 levels are correlated with body mass index (BMI) and triglycerides. These correlations could reflect genetic and/or environmental factors in common to PAI-1, triglycerides, and BMI. We applied multivariate genetic analysis methods to assess the relative importance of genetic and environmental influences on plasma PAI-1 levels and to test the significance of genetic and/or environmental influences shared by PAI-1, triglycerides, and BMI in 217 pairs of middle-aged and elderly twins, of whom 113 pairs were reared apart and 121 pairs were women. The heritability estimate for PAI-1 levels was 42%. Individual-specific environmental factors explained 36% of the variance for PAI-1 levels. The remaining variance of PAI-1 was explained by rearing and residual-familial environmental factors. Furthermore, a genetic correlation of 1.00 between PAI-1 and triglycerides, a rearing environmental correlation of 1.00 between PAI-1 and BMI, a residual-familial environmental correlation of 1.00 between PAI-1 and triglycerides, and a genetic correlation of 0.63 between PAI-1 and BMI, were found. In conclusion, the present results suggest that genetic influences on plasma PAI-1 are moderate. Genetic and shared rearing or residual-familial environmental factors shared by PAI-1, BMI, and triglycerides explain the phenotypic association between these measures. It appears that all the genetic influences for PAI-1 are more or less shared with those for triglycerides and BMI.


Key Words: genetic correlations • plasminogen activator inhibitor-1 • heritability • triglycerides • body mass index




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