Search Results
You are looking at 1 - 2 of 2 items for
- Author: Masahiro Okamoto x
- Refine by access: All content x
Search for other papers by Muneki Ikeda in
Google Scholar
PubMed
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Search for other papers by Yasushi Hojo in
Google Scholar
PubMed
Search for other papers by Yoshimasa Komatsuzaki in
Google Scholar
PubMed
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Search for other papers by Masahiro Okamoto in
Google Scholar
PubMed
Search for other papers by Asami Kato in
Google Scholar
PubMed
Search for other papers by Taishi Takeda in
Google Scholar
PubMed
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Department of Biophysics and Life Sciences, Bioinformatics Project of Japan Science and Technology Agency, Laboratory of Exercise Biochemistry and Neuroendocrinology, Department of Urology, Graduate School of Arts and Sciences, University of Tokyo, 3‐8‐1 Komaba, Meguro‐ku, Tokyo 152-8902, Japan
Search for other papers by Suguru Kawato in
Google Scholar
PubMed
The corticosterone (CORT) level changes along the circadian rhythm. Hippocampus is sensitive to CORT, since glucocorticoid receptors are highly expressed. In rat hippocampus fixed in a living state every 3 h, we found that the dendritic spine density of CA1 pyramidal neurons increased upon waking (within 3 h), as compared with the spine density in the sleep state. Particularly, the large-head spines increased. The observed change in the spine density may be due to the change in the hippocampal CORT level, since the CORT level at awake state (∼30 nM) in cerebrospinal fluid was higher than that at sleep state (∼3 nM), as observed from our earlier study. In adrenalectomized (ADX) rats, such a wake-induced increase of the spine density disappeared. S.c. administration of CORT into ADX rats rescued the decreased spine density. By using isolated hippocampal slices, we found that the application of 30 nM CORT increased the spine density within 1 h and that the spine increase was mediated via PKA, PKC, ERK MAPK, and LIMK signaling pathways. These findings suggest that the moderately rapid increase of the spine density on waking might mainly be caused by the CORT-driven kinase networks.
Search for other papers by Masami Hayashi in
Google Scholar
PubMed
Search for other papers by Masahiro Sakata in
Google Scholar
PubMed
Search for other papers by Takashi Takeda in
Google Scholar
PubMed
Search for other papers by Toshiya Yamamoto in
Google Scholar
PubMed
Search for other papers by Yoko Okamoto in
Google Scholar
PubMed
Search for other papers by Kenjiro Sawada in
Google Scholar
PubMed
Search for other papers by Akiko Kimura in
Google Scholar
PubMed
Search for other papers by Ryoko Minekawa in
Google Scholar
PubMed
Search for other papers by Masahiro Tahara in
Google Scholar
PubMed
Search for other papers by Keiichi Tasaka in
Google Scholar
PubMed
Search for other papers by Yuji Murata in
Google Scholar
PubMed
Glucose transporter 1 (GLUT1) plays an important role in the transport of glucose in the placenta. During early pregnancy, placentation occurs in a relatively hypoxic environment that is essential for appropriate embryonic development, and GLUT1 expression is enhanced in response to oxygen deficiency in the placenta. Hypoxia-inducible factor-1 (HIF-1)α is involved in the induction of GLUT1 expression in other cells. The present study was designed to test whether HIF-1α is involved in hypoxia-induced activation of GLUT1 expression using trophoblast-derived human BeWo and rat Rcho-1 cells as models. GLUT1 mRNA and protein expression were elevated under 5% O2 or in the presense of cobalt chloride, which has been shown to mimic hypoxia. Using rat GLUT1 (rGLUT1) promoter–luciferase constructs, we showed that this up-regulation was mediated at the transcriptional level. Deletion mutant analysis of the rGLUT1 promoter indicated that a 184 bp hypoxia-responsive element (HRE) of the promoter was essential to increase GLUT1 reporter gene expression in response to low-oxygen conditions. BeWo and Rcho-1 cells cultured under 5% O2 or with CoCl2 showed increased expression of HIF-1α protein compared with those cultured under 20% O2. To test whether this factor is directly involved in hypoxia-induced GLUT1 promoter activation, BeWo and Rcho-1 cells were transiently transfected with an HIF-1α expression vector. Exogeneous HIF-1α markedly increased the GLUT1 promoter activity from constructs containing the HRE site, while the GLUT1 promoter constructs lacking the HRE site were not activated by exogenous HIF-1α These data demonstrate that GLUT1 is up-regulated under 5% O2 or in the presence of CoCl2 in the placental cell lines through HIF-1α interaction with a consensus HRE site of the GLUT1 promoter.
