京都府立医科大学 松原弘明の不正

京都府立医科大学循環器内科、関西医科大学第二内科の松原弘明氏の論文での研究不正疑惑について(捏造・改竄・人体実験疑惑)

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関西医大から京都府立医大への道 【1】

2011-10-22 21:04:11 | 論文撤回Watch関連リンク
Retraction Watch / 2011.06.26 01:06 / 推薦数 : 5

雑誌Molecular and cellular biochemistry の2003, Volume 251, Numbers 1-2, Page 167 に論文撤回アナウンスが掲載されました。

Due to a mistake of duplicating the publication of original data which already appeared in Circulation Research (84: 1073–1084, 1999), the following paper published in Molecular Cellular Biochemistry has been retracted with an apology: Hiroaki Matsubara, Yasutaka Moriguchi, Yasukiyo Mori, Hiroya Masaki, Yoshiaki Tsutsumi, Yasunobu Shibasaki, Yoko Uchiyama-Tanaka, Schoichiro Fujiyama, Yoko Koyama, Atsuko Nose-Fujiyama, Satoshi Iba, Eriko Tateishi and Toshiji Iwasaka “Transactivation of EGF receptor induced by angiotensin II regulates fibronetic and TGF-β gene expression via transcriptional and post-transcriptional mechanisms”. Mol Cell Biochem 212: 187–201, 2000.

撤回された論文はすでにオンラインでは読めなくなっていますが、抄録のみオンラインで閲覧することは可能です。
Circulation Researchに掲載された先行論文の抄録と撤回論文の抄録を以下に併記します。少し長くなりますがお付き合い下さい。

Circ Res

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of a growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors.  Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and transforming growth factor-beta (TGF-beta) in cardiac fibroblasts.

Mol Cell Biochem

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors.  Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and TGF-beta in cardiac fibroblasts. 

 

Circ Res

Ang II stimulated fibronectin mRNA levels dose dependently, with a maximal increase ([=approximate]5-fold) observed after 12 hours of incubation.  Fibronectin synthesis induced by Ang II or calcium ionophore was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents.

Mol Cell Biochem

Ang II stimulated fibronectin mRNA levels dose-dependently with a maximal increase (approximately 5-fold) observed after 12 h of incubation.  Ang II-, or calcium ionophore-induced fibronectin synthesis was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents. 

 

Circ Res

Ang II-induced fibronectin mRNA was not affected by protein kinase C inhibitors or protein kinase C depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA.

Mol Cell Biochem

Ang II-induced fibronectin mRNA was not affected by PKC inhibitors or PKC depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA. 

 

Circ Res

We isolated the rat fibronectin gene, including the 5[prime]-flanking region, and found that  the activator protein-1 (AP-1) binding site present in the promoter region was responsible for the Ang II responsiveness of this gene.

Mol Cell Biochem

We isolated the rat fibronectin gene including the 5'-flanking region and found that  the AP-1 binding site present in the promoter region was responsible for the Ang II responsiveness of this gene. 

 

Circ Res

A gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-activating transcription factor (ATF)-2 antibodies.  Conditioned medium from Ang II-treated cells contained TGF-beta bioactivity, and addition of neutralizing TGF-beta antibody modestly (46%) inhibited induction of fibronectin.

Mol Cell Biochem

Gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-ATF-2 antibodies.  Conditioned medium from Ang II-treated cells contained TGF-beta bioactivity and addition of neutralizing TGF-beta antibody modestly (46%) inhibited induction of fibronectin.

 

Circ Res

Ang II-induced synthesis of TGF-beta was also abolished by inhibition of EGF-R function.  The effect of TGF-beta was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis.

Mol Cell Biochem

Ang II-induced synthesis of TGF-beta was also abolished by inhibition of EGF-R function.  The effect of TGF-beta was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis.  

 

Circ Res

We concluded that Ang II-induced expression of fibronectin and TGF-beta is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase and that Ang II-induced fibronectin mRNA expression is regulated by 2 different mechanisms, which are transcriptional control by binding of the c-fos/c-jun complex to the AP-1 site and posttranscriptional control by mRNA stabilization due to autocrine or paracrine effects of TGF-beta.  Thus, this study suggests that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade.

Mol Cell Biochem

We concluded that Ang II-induced expression of fibronectin and TGF-beta is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase, and that Ang II-induced fibronectin mRNA expression is regulated by two different mechanisms; transcriptional control by binding of c-fos/c-jun complex to the AP-1 site, and post-transcriptional control by mRNA stabilization due to autocrine and/or paracrine effects of TGF-beta.  Thus, this study suggested that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade.

 

だらだらと長くなりましたが、ということです。

全く同じと言ってよいかと思います。

撤回の理由が、 

a mistake of duplicating the publication

とありますが、要するに2重投稿と解釈してよいのではと思います。

さて撤回された論文が掲載された号は Control of Gene Expression by Catecholamines and the Renin-Angiotensin System を主題として特集が組まれています。いわゆる特別号(Special Issue)です。

特別号の場合は原稿の締め切りが普通はあります。

締め切りに間に合わず、やけっぱちになったのでしょうか?

特別号だからといって、過去に掲載されてものを再度掲載することは、許されているわけではありません。

論文撤回が発表されたのは2003年です。この2003年という年をよく覚えておいてください。

関西医大から京都府立医大への道 【2】に続きます。

 

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