| アイテムタイプ |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2025-01-14 |
| タイトル |
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タイトル |
GGT1 is a SNP eQTL gene involved in STAT3 activation and associated with the development of Post-ERCP pancreatitis |
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言語 |
en |
| 言語 |
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言語 |
eng |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 著者 |
Ryutaro Furukawa
Masaki Kuwatani
ing-Jing Jiang
Tanaka Yuki
Hasebe Rie
Kaoru Murakami
Kumiko Tanaka
Izuru Ohki
Ikuko Takahashi
Takeshi Yamasaki
Yuta Shinohara
Shunichiro Nozawa
Shintaro Hojyo
Shimpei I Kubota
Shigeru Hashimoto
Satoshi Hirano
Naoya Sakamoto
Murakami Masaaki
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| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Post-ERCP pancreatitis (PEP) is an acute pancreatitis caused by endoscopic-retrograde-cholangiopancreatography (ERCP). About 10% of patients develop PEP after ERCP. Here we show that gamma-glutamyltransferase 1 (GGT1)-SNP rs5751901 is an eQTL in pancreatic cells associated with PEP and a positive regulator of the IL-6 amplifier. More PEP patients had the GGT1 SNP rs5751901 risk allele (C) than that of non-PEP patients at Hokkaido University Hospital. Additionally, GGT1 expression and IL-6 amplifier activation were increased in PEP pancreas samples with the risk allele. A mechanistic analysis showed that IL-6-mediated STAT3 nuclear translocation and STAT3 phosphorylation were suppressed in GGT1-deficient cells. Furthermore, GGT1 directly associated with gp130, the signal-transducer of IL-6. Importantly, GGT1-deficiency suppressed inflammation development in a STAT3/NF-κB-dependent disease model. Thus, the risk allele of GGT1-SNP rs5751901 is involved in the pathogenesis of PEP via IL-6 amplifier activation. Therefore, the GGT1-STAT3 axis in pancreas may be a prognosis marker and therapeutic target for PEP. |
| 書誌情報 |
Scientific Report
巻 14,
号 1,
p. 12224,
発行日 2024-05
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| 出版者 |
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出版者 |
Springer Nature |
| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
2045-2322 |
| DOI |
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識別子タイプ |
DOI |
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関連識別子 |
10.1038/s41598-024-60312-2. |
