Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10765922 | Biochemical and Biophysical Research Communications | 2009 | 5 Pages |
Abstract
Hypoxemia is a common manifestation of various disorders and generates pressure overload to the heart. Here we analyzed the expression of lipocalin-type prostaglandin D synthase (L-PGDS) in the heart of C57BL/6 mice kept under normobaric hypoxia (10% O2) that generates hemodynamic stress. Northern and Western blot analyses revealed that the expression levels of L-PGDS mRNA and protein were significantly increased (>twofold) after 14Â days of hypoxia, compared to the mice kept under normoxia. Immunohistochemical analysis indicated that L-PGDS was increased in the myocardium of auricles and ventricles and the pulmonary venous myocardium at 28Â days of hypoxia. Moreover, using C57BL/6 mice lacking heme oxygenase-2 (HO-2â/â), a model of chronic hypoxemia, we showed that the expression level of L-PGDS protein was twofold higher in the heart than that of wild-type mouse. L-PGDS expression is induced in the myocardium under hypoxemia, which may reflect the adaptation to the hemodynamic stress.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Biochemistry
Authors
Feng Han, Kazuhisa Takeda, Kazunobu Ishikawa, Masao Ono, Fumiko Date, Satoru Yokoyama, Kazumichi Furuyama, Yotaro Shinozawa, Yoshihiro Urade, Shigeki Shibahara,