TY - JOUR
T1 - SNPs in BRAP associated with risk of myocardial infarction in Asian populations
AU - Ozaki, Kouichi
AU - Sato, Hiroshi
AU - Inoue, Katsumi
AU - Tsunoda, Tatsuhiko
AU - Sakata, Yasuhiko
AU - Mizuno, Hiroya
AU - Lin, Tsung Hsien
AU - Miyamoto, Yoshinari
AU - Aoki, Asako
AU - Onouchi, Yoshihiro
AU - Sheu, Sheng Hsiung
AU - Ikegawa, Shiro
AU - Odashiro, Keita
AU - Nobuyoshi, Masakiyo
AU - Juo, Suh Hang H.
AU - Hori, Masatsugu
AU - Nakamura, Yusuke
AU - Tanaka, Toshihiro
N1 - Funding Information:
We thank M. Takahashi, M. Yoshii, S. Abiko, W. Yamanobe, R. Ohishi, M. Watabe and T. Furusho for their assistance. We also thank all the other members of Center for Genomic Medicine, RIKEN and OACIS for their contribution to the completion of our study. We are also grateful to members of The Rotary Club of Osaka-Midosuji District 2660 Rotary International in Japan for supporting our study. This work was supported in part by grants from the Takeda Science Foundation, the Uehara Science Foundation, the Japanese Millennium Project and the Ministry of Education, Science, Sports, Culture and Technology of Japan and NHRI-Ex96-9607PI (Taiwan).
PY - 2009/3
Y1 - 2009/3
N2 - Myocardial infarction is a common disease and among the leading causes of death in the world. We previously reported association of variants in LGALS2, encoding galectin-2, with myocardial infarction susceptibility in a case-control association study in a Japanese population. Here we identify BRAP (BRCA1-associated protein) as a galectin-2-binding protein. We report an association of SNPs in BRAP with myocardial infarction risk in a large Japanese cohort (P = 3.0 × 10-18, OR = 1.48, 2,475 cases and 2,778 controls), with replication in additional Japanese and Taiwanese cohorts (P = 4.4 × 10-6, 862 cases and 1,113 controls and P = 4.7 × 10-3, 349 cases and 994 controls, respectively). BRAP expression was observed in smooth muscle cells (SMCs) and macrophages in human atherosclerotic lesions. BRAP knockdown by siRNA using cultured coronary endothelial cells suppressed activation of NF-κB, a central mediator of inflammation.
AB - Myocardial infarction is a common disease and among the leading causes of death in the world. We previously reported association of variants in LGALS2, encoding galectin-2, with myocardial infarction susceptibility in a case-control association study in a Japanese population. Here we identify BRAP (BRCA1-associated protein) as a galectin-2-binding protein. We report an association of SNPs in BRAP with myocardial infarction risk in a large Japanese cohort (P = 3.0 × 10-18, OR = 1.48, 2,475 cases and 2,778 controls), with replication in additional Japanese and Taiwanese cohorts (P = 4.4 × 10-6, 862 cases and 1,113 controls and P = 4.7 × 10-3, 349 cases and 994 controls, respectively). BRAP expression was observed in smooth muscle cells (SMCs) and macrophages in human atherosclerotic lesions. BRAP knockdown by siRNA using cultured coronary endothelial cells suppressed activation of NF-κB, a central mediator of inflammation.
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U2 - 10.1038/ng.326
DO - 10.1038/ng.326
M3 - Article
C2 - 19198608
AN - SCOPUS:61349108698
SN - 1061-4036
VL - 41
SP - 329
EP - 333
JO - Nature Genetics
JF - Nature Genetics
IS - 3
ER -
