Author Fujita, Hirofumi| Shiosaka, Masahiko| Ogino, Tetsuya| Okimura, Yuya| Utsumi, Toshihiko| Sato, Eisuke F.| Akagi, Reiko| Inoue, Masayasu| Utsumi, Kozo| Sasaki, Junzo|
Published Date 2008-06-23
Publication Title Brain Research
Volume volume1206
Content Type Journal Article
Author Kobuchi, Hirotsugu| Moriya, Koko| Ogino, Tetsuya| Fujita, Hirofumi| Inoue, Keiji| Shuin, Taro| Yasuda, Tatsuji| Utsumi, Kozo| Utsumi, Toshihiko|
Published Date 2012-11-26
Publication Title PLoS ONE
Volume volume7
Issue issue11
Content Type Journal Article
FullText URL fulltext.pdf
Author Kanzaki, Yuki| Fujita, Hirofumi| Sato, Keita| Hosokawa, Mio| Matsumae, Hiroshi| Shiraga, Fumio| Morizane, Yuki| Ohuchi, Hideyo|
Keywords Kir7.1 KCNJ13 human-induced pluripotent cells retinal pigment epithelium phagocytosis
Published Date 2020-05
Publication Title Investigative Ophthalmology & Visual Science
Volume volume61
Issue issue5
Publisher Association for Research in Vision and Ophthalmology
Start Page 38
ISSN 0146-0404
NCID AA00683736
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders Copyright 2020 The Authors
File Version publisher
PubMed ID 32437550
DOI 10.1167/iovs.61.5.38
Web of Science KeyUT 000540905500039
Related Url isVersionOf https://doi.org/10.1167/iovs.61.5.38
JaLCDOI 10.18926/AMO/50408
FullText URL 67_3_153.pdf
Author Yamamoto, Masanao| Fujita, Hirofumi| Katase, Naoki| Inoue, Keiji| Nagatsuka, Hitoshi| Utsumi, Kozo| Sasaki, Junzo| Ohuchi, Hideyo|
Abstract Ever since protoporphyrin IX (PpIX) was discovered to accumulate preferentially in cancer cells after 5-aminolevulinic acid (ALA) treatment, photodynamic treatment or therapy (PDT) has been developed as an exciting new treatment option for cancer patients. However, the level of PpIX accumulation in oral cancer is fairly low and insufficient for PDT. Ferrochelatase (FECH) and ATP-binding cassette transporter G2 (ABCG2) are known to regulate PpIX accumulation. In addition, serum enhances PpIX export by ABCG2. We investigated here whether and how inhibitors of FECH and ABCG2 and their combination could improve PpIX accumulation and PDT efficacy in an oral cancer cell line in serum-containing medium. ABCG2 inhibitor and the combination of ABCG2 and FECH inhibitors increased PpIX in the presence of fetal bovine serum (FBS) in an oral cancer cell line. Analysis of ABCG2 gene silencing also revealed the involvement of ABCG2 in the regulation of PpIX accumulation. Inhibitors of FECH and ABCG2, and their combination increased the efficiency of ALA-PDT even in the presence of FBS. ALA-PDT-induced cell death was accompanied by apoptotic events and lipid peroxidation. These results suggest that accumulation of PpIX is determined by the activities of ABCG2 and FECH and that treatment with a combination of their inhibitors improves the efficacy of PDT for oral cancer, especially in the presence of serum.
Keywords 5-aminolevulinic acid protoporphyrin IX oncology photodynamic therapy apoptosis
Amo Type Original Article
Published Date 2013-06
Publication Title Acta Medica Okayama
Volume volume67
Issue issue3
Publisher Okayama University Medical School
Start Page 153
End Page 164
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23804138
Web of Science KeyUT 000320747900004
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/50681
FullText URL fulltext.pdf
Author Habuta, Munenori| Yasue, Akihiro| Suzuki, Ken-Ichi T.| Fujita, Hirofumi| Sato, Keita| Kono, Hitomi| Takayama, Ayuko| Bando, Tetsuya| Miyaishi, Satoru| Oyadomari, Seiichi| Tanaka, Eiji| Ohuchi, Hideyo|
Published Date 2020-10-15
Publication Title PLoS ONE
Volume volume15
Issue issue10
Publisher Public Library of Science
Start Page e0240333
ISSN 1932-6203
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2020 Habuta et al.
File Version publisher
PubMed ID 33057360
DOI 10.1371/journal.pone.0240333
Web of Science KeyUT 000581814700082
Related Url isVersionOf https://doi.org/10.1371/journal.pone.0240333
JaLCDOI 10.18926/AMO/59950
FullText URL 74_3_199.pdf
Author Fujita, Hirofumi| Bando, Tetsuya| Oyadomari, Seiichi| Ochiai, Kazuhiko| Watanabe, Masami| Kumon, Hiromi| Ohuchi, Hideyo|
Abstract Dickkopf 3 (Dkk3) is a secreted protein belonging to the Dkk family and encoded by the orthologous gene of REIC. Dkk3/REIC is expressed by mouse and human adrenal glands, but the understanding of its roles in this organ is still limited. To determine the functions of Dkk3 in the mouse adrenal gland, we first identified that the mouse Dkk3 protein is N-glycosylated in the adrenal gland as well as in the brain. We performed proteome analysis on adrenal glands from Dkk3-null mice, in which exons 5 and 6 of the Dkk3 gene are deleted. Twodimensional polyacrylamide gel electrophoresis of adrenal proteins from wild-type and Dkk3-null mice revealed 5 protein spots whose intensities were altered between the 2 genotypes. Mass spectrometry analysis of these spots identified binding immunoglobulin protein (BiP), an endoplasmic reticulum (ER) chaperone. To determine whether mouse Dkk3 is involved in the unfolded protein response (UPR), we carried out a reporter assay using ER-stress responsive elements. Forced expression of Dkk3 resulted in the induction of distinct levels of reporter expression, showing the UPR initiated by the ER membrane proteins of activating transcription factor 6 (ATF6) and inositol-requring enzyme 1 (IRE1). Thus, it is possible that Dkk3 is a physiological ER stressor in the mouse adrenal gland.
Keywords Dkk3 knockout mouse adrenal gland glucose-regulated protein 78 proteome endoplasmic reticulum stress
Amo Type Original Article
Published Date 2020-06
Publication Title Acta Medica Okayama
Volume volume74
Issue issue3
Publisher Okayama University Medical School
Start Page 199
End Page 208
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2020 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 32577017
Web of Science KeyUT 000543363400003
NAID 120006862792