JaLCDOI 10.18926/AMO/53521
FullText URL 69_3_145.pdf
Author Ishii, Hiroko| Kamikawa, Shigeshi| Hirohata, Satoshi| Mizutani, Akifumi| Abe, Koji| Seno, Masaharu| Oohashi, Toshitaka| Ninomiya, Yoshifumi|
Abstract Eosinophil cationic protein (ECP) is well known as a cationic protein contained in the basic granules of activated eosinophils. Recent studies have reported that ECP exhibits novel activities on various types of cells, including rat neonatal cardiomyocytes. Here we evaluated the effects of ECP on rat cardiac myoblast H9c2 cells. Our results showed that ECP enhanced the survival of the cells, in part by promoting the ERK and Akt/GSK-3β signaling pathways. ECP attenuated the cytotoxic effects of H2O2 on H9c2 cells as well as the production of reactive oxygen species, the number of apoptotic cells and caspase 3/7 activity in the cells. In conclusion, ECP activated the ERK and Akt/GSK-3β pathways, resulting in anti-oxidative effects on H9c2 cells that attenuated apoptosis.
Keywords ECP reactive oxygen species Akt ERK
Amo Type Original Article
Published Date 2015-06
Publication Title Acta Medica Okayama
Volume volume69
Issue issue3
Publisher Okayama University Medical School
Start Page 145
End Page 153
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 26101190
Web of Sience KeyUT 000356903000003
Author Toeda, Kenichi| Nakamura, Keigo| Hirohata, Satoshi| Hatipoglu, Omer F.| Demircan, Kadir| Yamawaki, Hitoshi| Ogawa, Hiroko| Kusachi, Shozo| Shiratori, Yasushi| Ninomiya, Yoshifumi|
Published Date 2005-12
Publication Title Molecular and Cellular Biochemistry
Volume volume280
Issue issue1-2
Content Type Journal Article
Author Demircan, Kadir| Hirohata, Satoshi| Nishida, Keiichiro| Hatipoglu, Omer F.| Oohashi, Toshitaka| Yonezawa, Tomoko| Apte, Suneel S.| Ninomiya, Yoshifumi|
Published Date 2005-5
Publication Title Arthritis & Rheumatism
Volume volume52
Issue issue5
Content Type Journal Article
JaLCDOI 10.18926/AMO/31831
FullText URL fulltext.pdf
Author Hatipoglu, Omer Faruk| Hirohata, Satoshi| Yaykasli, Kursat Oguz| Cilek, Mehmet Zeynel| Demircan, Kadir| Shinohata, Ryoko| Yonezawa, Tomoko| Oohashi, Toshitaka| Kusachi, Shozo| Ninomiya, Yoshifumi|
Abstract <p>ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin motifs 1) is an inflammatory-induced gene. We have previously reported that ADAMTS1 was strongly but transiently expressed in the infarcted heart. In this study, we investigated whether a 3'-untranslated region (UTR) affects the mRNA stability of this gene. When stimulated with tissue necrosis factor (TNF)-alpha, the expression level of ADAMTS1 mRNA rapidly increased, but the induction of ADAMTS1 mRNA peaked at 6h after stimulation, after which the expression levels of ADAMTS1 mRNA decreased. The 3'-UTR ADAMTS1 mRNA contains multiple adenine and uridine-rich elements, suggesting that the 3'-UTR may regulate gene stability. The addition of actinomycin D, an RNA synthesis inhibitor, demonstrated the decay of induced ADAMTS1 mRNA by TNF-alpha. Furthermore, a region containing multiple AUUUA motifs within the ADAMTS1 3'-UTR destabilized transfected Enhanced Green Fluorescence Protein (EGFP) mRNA expression. These results demonstrated that the ADAMTS1 3'-UTR may regulate the expression of ADAMTS1 mRNA.</p>
Keywords ADAMTS1 gene regulation metalloproteinase
Amo Type Original Article
Published Date 2009-04
Publication Title Acta Medica Okayama
Volume volume63
Issue issue2
Publisher Okayama University Medical School
Start Page 79
End Page 85
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 19404339
Web of Sience KeyUT 000265457600002
Author 廣畑 聡|
Published Date 1997-03-25
Publication Title
Content Type Thesis or Dissertation