Katsumi Fukamachi
University of Shizuoka
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Featured researches published by Katsumi Fukamachi.
Molecular Brain Research | 1999
Kiyomitsu Nemoto; Masashi Sekimoto; Katsumi Fukamachi; Fumiko Nemoto; Shingo Miyata; Yoshiyuki Nakamura; Masanori Hamada; Emiko Senba; Takashi Ueyama; Masakuni Degawa
We have previously reported that in cultured rat vascular smooth muscle cells (VSMCs), neurotrophin-3 (NT-3) gene expression was suppressed by TPA (12-O-tetradecanoyl phorbol-13-acetate), which induces an AP-1 transcription factor. In the present study, to clarify the mechanism for TPA-mediated downregulation of NT-3 gene expression, effects of cycloheximide and dexamethasone (Dex) on the TPA-mediated downregulation were examined in VSMCs. Pretreatment with cycloheximide, an inhibitor of protein synthesis, or simultaneous treatment with Dex, an inhibitor of AP-1, suppressed the TPA-mediated downregulation of NT-3 gene expression. Furthermore, co-transfection of c-fos and c-jun expression vectors into VSMCs resulted in decrease in the NT-3 gene expression. The present findings suggest that TPA-induced AP-1 de novo synthesis causes the downregulation of NT-3 gene expression in VSMCs.
Neuroscience Letters | 1996
Kiyomitsu Nemoto; Haruaki Kageyama; Takashi Ueyama; Katsumi Fukamachi; Masashi Sekimoto; Isao Tomita; Emiko Senba; Cynthia J. Forehand; Edith D. Hendley
We previously reported a missense mutation in the low affinity nerve growth factor receptor (LNGFR) gene of spontaneously hypertensive rats (SHR), proposing this gene as a promising candidate in genetic hypertension. In this study we provide further support for implicating this gene in genetic hypertension using two new inbred strains, WKHT and WKHA rats. These strains originated from crossbreeding SHR rats with normotensive Wistar-Kyoto rats (WKY): WKHT rats are hypertensive but not hyperactive, and WKHA rats are hyperactive but not hypertensive. Nucleotide sequence analysis of the LNGFR gene revealed that WKHT has the same mutation as SHR, whereas WKHA has the normal sequence, as seen in WKY. These results support our original hypothesis that the mutated LNGFR gene is linked to hypertension, since the mutation had co-segregated with the hypertensive trait, and not hyperactivity trait of SHR.
Neuroreport | 1998
Masashi Sekimoto; Katsumi Fukamachi; Fumiko Nemoto; Shingo Miyata; Masakuni Degawa; Emiko Senba; Takashi Ueyama; Kiyomitsu Nemoto
THE neurotrophin-3 (NT-3) gene has previously been reported to consist of three exons including two 5′ short untranslated exons and a 3′ long exon encoding the entire protein, and to give rise to two classes of transcripts by alternative splicing of the 5′ exons to the 3′ coding exon. In the present study, we demonstrated the presence of at least four new classes of transcripts of the NT-3 gene, in addition to the two known transcripts. The present finding proposes the further complexity of the regulational mechanism for NT-3 expression.
Hypertension Research | 2005
Kiyomitsu Nemoto; Masashi Sekimoto; Katsumi Fukamachi; Haruaki Kageyama; Masakuni Degawa; Masanori Hamada; Edith D. Hendley; I. Mhairi Macrae; James S. Clark; Anna F. Dominiczak; Takashi Ueyama
Sympathetic hyper-innervation and increased levels of nerve growth factor (NGF), an essential neurotrophic factor for sympathetic neurons, have been observed in the vascular tissues of spontaneously hypertensive rats (SHRs). Such observations have suggested that the pathogenesis of hypertension might involve a qualitative or quantitative abnormality in the NGF protein, resulting from a significant mutation in the genes promoter or coding region. In the present study, we analyzed the nucleotide sequences of the cis-element of the NGF gene in SHRs, stroke-prone SHRs (SHRSPs), and normotensive Wistar-Kyoto (WKY) rats. The present analyses revealed some differences in the 3-kb promoter region, coding exon, and 3′ untranslated region (3′UTR) for the NGF gene among those strains. However, the observed differences did not lead to changes in promoter activity or to amino acid substitution; nor did they represent a link between the 3′UTR mutation of SHRSPs and elevated blood pressure in an F2 generation produced by crossbreeding SHRSPs with WKY rats. These results suggest that the NGF gene locus is not involved in hypertension in SHR/SHRSP strains. The present study also revealed two differences between SHRs and WKY rats, as found in cultured vascular smooth muscle cells and in mRNA prepared from each strain. First, SHRs had higher expression levels of c-fos and c-jun genes, which encode the component of the AP-1 transcription factor that activates NGF gene transcription. Second, NGF mRNAs prepared from SHRs had a longer 3′UTR than those prepared from WKY rats. Although it remains to be determined whether these events play a role in the hypertension of SHR/SHRSP strains, the present results emphasize the importance of actively searching for aberrant trans-acting factor(s) leading to the enhanced expression of the NGF gene and NGF protein in SHR/SHRSP strains.
Biochemical and Biophysical Research Communications | 1998
Kiyomitsu Nemoto; Katsumi Fukamachi; Fumiko Nemoto; Shingo Miyata; Masanori Hamada; Yoshiyuki Nakamura; Emiko Senba; Takashi Ueyama
Biochemical and Biophysical Research Communications | 1996
Haruaki Kageyama; Kiyomitsu Nemoto; Fumiko Nemoto; Masashi Sekimoto; Yasuo Nara; Tohru Nabika; Yoshimi Iwayama; Katsumi Fukamachi; Isao Tomita; Emiko Senba; Cynthia J. Forehand; Edith D. Hendley; Takashi Ueyama
Japanese Heart Journal | 1998
Katsumi Fukamachi; Kiyomitsu Nemoto; Takashi Ueyama; Yoshimi Iwayama; Masashi Sekimoto; Masanori Hamada; Edith D. Hendley; Takako Tomita; Isao Tomita
Japanese Heart Journal | 1998
Masashi Sekimoto; Kiyomitsu Nemoto; Takashi Ueyama; Katsumi Fukamachi; Masanori Hamada; Anna F. Dominiczak; Takako Tomita; Isao Tomita
The Keio Journal of Medicine | 1997
Kiyomitsu Nemoto; Katsumi Fukamachi; Emiko Senba; Takashi Ueyama
Japanese Heart Journal | 1997
Masashi Sekimoto; Takashi Ueyama; Kiyomitsu Nemoto; Haruaki Kageyama; Katsumi Fukamachi; Isao Tomita; Emiko Senba; Yasuo Nara; Katsumi Ikeda; Yukio Yamori