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Table of Contents
Vol. 32, No. 5, 2011
Issue release date: November 2011
Section title: Original Paper
Cerebrovasc Dis 2011;32:489–496
(DOI:10.1159/000331921)

Contribution of Cystatin C Gene Polymorphisms to Cerebral White Matter Lesions

Mitaki S.a · Nagai A.b · Sheikh A.M.b · Terashima M.d · Isomura M.c · Nabika T.c · Yamaguchi S.a
Departments of aNeurology, bLaboratory Medicine and cFunctional Pathology, Shimane University School of Medicine, Izumo, and dDepartment of Registered Dietitian and Nutritional Science, Tokaigakuen University Faculty of Human Wellness, Nagoya, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: December 13, 2010
Accepted: August 02, 2011
Published online: November 01, 2011
Issue release date: November 2011

Number of Print Pages: 8
Number of Figures: 1
Number of Tables: 5

ISSN: 1015-9770 (Print)
eISSN: 1421-9786 (Online)

For additional information: http://www.karger.com/CED

Abstract

Background: Vascular remodeling plays an important role in the development of arteriosclerosis and any of the resulting white matter lesions in the brain. An imbalance between cysteine proteases and the cysteine protease inhibitor cystatin C (CST3) may exacerbate vascular remodeling through degradation of extracellular matrix proteins. Therefore, we evaluated the association between functional polymorphisms in the CST3 gene and the development of cerebral white matter lesions. Methods: In a total of 2,676 participants, 3 CST3 genepolymorphisms were genotyped in 92 cases with severe deep white matter hyperintensity (DWMH), and 184 subjects were randomly selected age- and sex-matched controls without any signs of DWMH. The genetic effects of these polymorphisms on DWMH and plasma CST3 levels were examined. CST3 expression vectors were transfected into an astrocytoma cell line and the expression level of CST3 mRNA was analyzed by quantitative RT-PCR. Intracellular and secreted levels of CST3 in the cell culture were quantified by Western blot and ELISA, respectively. Results: A significant association was found between one CST3 gene haplotype and DWMH (p = 0.002). This haplotype was also associated with lower plasma CST3 levels (p = 0.01). An in vitro transfection study revealed that the +148A allele, which is included in the risk haplotype, significantly reduced the secretion and increased the intracellular accumulation of CST3; however, it had no effect on the mRNA expression. Conclusions: Our study shows that polymorphisms in the CST3 gene are significantly associated with the likelihood of DWMH. Substitution of A for G at +148 of the CST3 gene decreased the extracellular availability of CST3 in vitro, which might result in the activation of protease activity.

© 2011 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: December 13, 2010
Accepted: August 02, 2011
Published online: November 01, 2011
Issue release date: November 2011

Number of Print Pages: 8
Number of Figures: 1
Number of Tables: 5

ISSN: 1015-9770 (Print)
eISSN: 1421-9786 (Online)

For additional information: http://www.karger.com/CED


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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