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Prepublished online as a Blood First Edition Paper on May 1, 2003; DOI 10.1182/blood-2002-12-3733.
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Blood, 1 September 2003, Vol. 102, No. 5, pp. 1619-1621
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC
TRIALS
Brief report
Microsatellite polymorphism in heme oxygenase-1 gene promoter is associated with susceptibility to oxidant-induced apoptosis in lymphoblastoid cell lines
Hisao Hirai,
Hiroshi Kubo,
Mutsuo Yamaya,
Katsutoshi Nakayama,
Muneo Numasaki,
Seiichi Kobayashi,
Satoshi Suzuki,
Shigeki Shibahara, and
Hidetada Sasaki
From the Departments of Geriatric and Respiratory Medicine, Tohoku
University School of Medicine; Department of Thoracic Surgery, Institute of
Development, Aging and Cancer, Tohoku University; and Molecular Biology and
Applied Physiology, Tohoku University School of Medicine, Sendai, Japan.
Heme oxygenase-1 (HO-1) confers cytoprotection against oxidative stress. A
(GT)n dinucleotide repeat in the 5'-flanking region of human HO-1 gene
shows length polymorphism, which was classified into S (< 27 GT), M (27-32
GT), and L alleles ( 33 GT). Polymorphism in the HO-1 gene promoter was
shown to be associated with susceptibility to pulmonary emphysema and
restenosis after angioplasty. However, the biologic mechanism underlying these
associations is still unclear. To examine this issue, we established
lymphoblastoid cell lines (LCLs) from subjects possessing S/S or L/L
genotypes. HO-1 mRNA expressions and HO activities induced by oxidative stress
were significantly higher in LCLs with S/S than those with L/L. Furthermore,
LCLs with S/S were significantly more resistant to oxidant-induced apoptosis
than those with L/L. These findings suggested that the polymorphism of the
HO-1 gene is associated with the strength of antiapoptotic effects of HO-1,
resulting in an association with susceptibility to oxidative
stress–mediated diseases.
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