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Induction of lipocalin-type prostaglandin D synthase in mouse heart under hypoxemia |
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| Authors: | Feng Han Kazuhisa Takeda Masao Ono Satoru Yokoyama Yotaro Shinozawa Shigeki Shibahara |
| Institution: | a Department of Molecular Biology and Applied Physiology, Tohoku University School of Medicine, Sendai 980-8575, Japan b Department of Emergency and Critical Care Medicine, Tohoku University School of Medicine, Sendai 980-8575, Japan c First Department of Internal Medicine, Fukushima Medical University, Fukushima, Japan d Division of Histopathology, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan e Department of Molecular Behavioral Biology, Osaka Bioscience Institute, Osaka, Japan |
| 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 14 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 28 days of hypoxia. Moreover, using C57BL/6 mice lacking heme oxygenase-2 (HO-2−/−), 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. |
| Keywords: | Prostaglandin D synthase Heme oxygenase Hypoxia Prostaglandin D2 Lung Heart Pulmonary venous myocardium |
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