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in Circulation Research (84: 1073–1084, 1999), the following paper published in Molecular Cellular Biochemistry has been retracted with an apology: Hiroaki Matsubara, Yasutaka Moriguchi, Yasukiyo Mori, Hiroya Masaki, Yoshiaki Tsutsumi, Yasunobu Shibasaki, Yoko Uchiyama-Tanaka, Schoichiro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。
Retraction Watch / 2011.06.27 01:01 / 推薦数 : 3
関西医大から京都府立医大への道 【1】よりの続きです。
雑誌Hypertenstionに2003年に掲載された論文を紹介します。
11名の著者からなる論文で、責任著者は当時関西医大の内科に所属し、前回紹介した撤回論文の筆頭著者でもあります。
この論文中の図が誤って掲載されていたとして2004年に訂正のアナウンスがされました。
何がどう誤っていたのでしょうか？
訂正前の図を下に示します。
ある図をひっくり返すと別の図にそっくりになります。なぜ、こんな「誤り」がおきたのかは不明です。
著者らが自ら、「誤り」にきづいたのか、
あるいは
著者らが、受動的に、「誤り」にきづかされたのか
（すなわち、第3者が雑誌社に連絡、雑誌社から著者らに連絡）
も、不明です。
関西医大から京都府立医大への道 【3】に続きます。
Retraction Watch / 2011.06.28 08:29 / 推薦数 : 5
関西医大から京都府立医大への道 【2】からの続きです。
今回は次の二つの論文の読みくらべです。
一つ目は雑誌Biochemical and Biophysical Research Communicationsに掲載された論文（以下BBRC 論文とします）。
対抗するのは雑誌 Hypertensionに掲載のもの（以下Hypertension 論文）。
両論文とも2001年の掲載です。
BBRC 論文の筆頭著者は責任著者も兼ねています。
当時関西医大内科に属していたこの著者はHypertension 論文ではセカンドですが責任著者をつとめています。
BBRC These differences might be due to variation of cell types or reflect the complexity of the network involved in negative regulation of ERK activity. Thus, further dissection of the AT2 signaling pathway and identification of cross-point with Pyk2-JNK intracellular cascade, may provide new perspectives for pharmacological targeting of proliferative diseases.
Hypertension These differences might be due to a variation of cell types or might reflect the complexity of the network involved in negative regulation of ERK activity. Thus, further dissection of the AT2 signaling pathway and identification of the cross-point with EGFR cascades may provide new perspectives for pharmacological targeting of proliferative diseases and a unique example of negative cross-talk in growth signals.
BBRC However, the molecules interacting with SHP-1 were not defined in these earlier studies. Interestingly, Li et al. reported that platelet thrombin receptor causes SHP-1 tyrosine-phosphorylation in a PTX dependent manner, and suggested the role of tyrosine kinases linked to the thrombin receptor by Gi-protein.
Hypertension However, the molecules interacting with SHP-1 were not defined in these earlier studies. Li et al reported that platelet thrombin receptor causes SHP-1 tyrosine phosphorylation in a PTX-dependent manner and suggested the role of tyrosine kinases linked to the thrombin receptor by Gi protein.
BBRC Recently, a structural model for SHP-1 was proposed, in which SH2 domains of SHP-1 were shown to be capable of interacting with its C terminus in a phosphotyrosine-dependent manner and thereby drive the PTPase domain in an inactive conformation.
Hypertension Recently, a structural model for SHP-1 was proposed in which SH2 domains of SHP-1 were shown to be capable of interacting with its C terminus in a phosphotyrosine-dependent manner and thereby drive the PTPase domain in an inactive conformation.
BBRC It is possible that the conformational change of SHP-1 induced by AT2 causes an increased association of SHP-1 with downstream molecules of Pyk2, leading to JNK inactivation. Thus, we speculated that AT2 has the capacity to disrupt this intramolecular interaction.
Hypertension It is possible that the conformational change of SHP-1 induced by AT2 leads to the increased association of SHP-1 with EGFR and forms the basis for activation toward the receptor as observed in our study. Thus, AT2 may have the capacity to disrupt this intramolecular interaction.
BBRC SHP-1 is predominantly expressed in hematopoietic cells and plays a key role in hematopoiesis. Although the role of SHP-1 in VSMC has not been defined in detail, the present study suggested a novel function of SHP-1 in AT2-mediated JNK inactivation followed by a growth inhibitory action.
Hypertension SHP-1 is predominantly expressed in hematopoietic cells and plays a key role in hematopoiesis. Although the role of SHP-1 in VSMCs has not been defined in detail, the present study suggested a novel function of SHP-1 in AT2-mediated ERGFR inactivation followed by a growth inhibitory action.
BBRC Since SHP-1 was reported to interact with SHP-2, further studies are required to define the relationship between SHP-1 and SHP-2 in the mechanism for AT2 activation.
Hypertension Because SHP-1 was reported to interact with SHP-2, further studies are required to define the relationship between SHP-1 and SHP-2 in the mechanism of AT2 activation.
まただらだらと長くなりましたが、以上両論文の一部を読みくらべて、いかが思われましたか？
関西医大から京都府立医大への道 【4】に続きます。
Retraction Watch / 2011.06.30 03:09 / 推薦数 : 3
前回は2つの論文を (BBRC 論文とHypertension 論文) 読みくらべましたが、
今回は両論文中の図を見てみましょう
。
大変よく似ています。
さらに、両論文中の表も比較してみましょう。
ちなみにBBRC論文はHypertension論文の掲載許可がでてから投稿されているようです。
関西医大から京都府立医大への道 【5】に続きます。
【5】関西医大から京都府立医大への道
Retraction Watch / 2011.07.01 00:13 / 推薦数 : 2
【4】関西医大から京都府立医大への道 よりの続きです。
今回は二つの論文をくらべませんが、ひとつの論文中の図を見くらべます。
BBRCに掲載された論文中の図を下に示します。
この2つの図は大変よく似ています。
細かいギザギザまでほんとにそっくりで、しびれてしまいました。
Hypertension論文で図に「誤り」があり、訂正のアナウンスがなされたことはとりあげたばかりです。
この図にも、訂正のアナウンスがでるのでしょうか？
10年たった今、訂正のアナウンスがなされたら、
拍手喝采
ものだと思います。
へ続きます。
【6】関西医大から京都府立医大への道
Retraction Watch / 2011.07.02 00:02 / 推薦数 : 4
【3】関西医大から京都府立医大への道 では同じ研究グループからの2つの論文を読みくらべましたが、
今回の2つの論文は別々の施設からの発表です。
先発論文は1998年イスラエルのグループからの発表。
対する後発論文は2000年おなじみ関西医大のグループです。
関西医大 The delayed response of JNK suggested that JNK is involved in a later stage of transcription regulation and suggests that the signaling machinery involved in the activation of JNK is different from that leading to ERK activation. Our results suggested that Ang II binding to AT1-R triggers the activation of Ca2+ signaling and PKC. The signal is then transmitted to the Pyk2 and further to the small G protein Rac1 but not Cdc42, although the direct activation of Rac1 by Pyk2 is not proved in this study.
イスラエル The delayed response of JNK observed here (Fig. 1) may indicate that JNK is involved in a later stage of transcription regulation and suggests that the signaling machinery that is involved in the activation of JNK is different from that leading to ERK activation. This upstream machinery was elucidated in this study, and our results suggest that GnRH binding to its receptors triggers the activation ofPKC, which occurs most probably via the heterotrimeric Gq protein and PLC. The signal is then transmitted to a Src-family PTK and further to the sGPs CDC42 and possibly Rac1.
関西医大 Although in many cases Rac1 and Cdc42 use similar guanine nucleotide exchange factors, the effect of Cdc42 on Ang II-JNK pathway seems to be limited. Similar phenomena were reported for serum-induced proliferation and JNK activation by gonadotropin-released hormone. Thus, the activation of JNK by Ang II in cardiac fibroblasts involves Ras-independent activation of Rac1 by Pyk2.
イスラエル Although in many cases CDC42 and Rac1 seem to use similar guanine nucleotide exchange factors, the effect of Rac1 on the GnRH-JNK pathway seems to be limited. Similar phenomenon, where CDC42 transmits downstream signals without the involvement of Rac1, was recently reported for serum-induced proliferation. Ha-Ras does not seem to be significantly involved in GnRH-induced signaling that contributes to the JNK cascade.
関西医大 The ERK cascade is not the only route by which Ang II communicates with the nucleus. Here, the JNK pathway was shown to be activated in response to Ang II, to a much greater extent than the ERK cascade.
イスラエル However, the ERK cascade is not the only route by which GnRH communicates with the nucleus. Here the JNK pathway is shown to be significantly activated in response to GnRH-a, to a much greater extent than the ERK cascade.
かなり専門的な同じ分野のことを書くと、これぐらいよく似たものに自然になっちゃう、こともあり得ます？
【7】関西医大から京都府立医大への道 へ続きます。
Retraction Watch / 2011.07.03 00:40 / 推薦数 : 4
今回でシリーズ7回目。
6回目までは、ずっと関西医大発の論文でしたが、今回ようやく京都府立医大にたどりつきました。
後発論文は2005年京都府立医大のグループよりの発表です。
京府医大 Previous investigations have provided inferential evidence that biological processes modulated by NO might extend to include angiogenesis.
関西医大 Previous investigations have provided inferential evidence that biological processes modulated by NO might extend to include angiogenesis.
京府医大 We have also reported that overexpression of endothelial NO synthase (eNOS) causes a marked increase in neocapillary formation in response to tissue ischemia.
関西医大 Our study demonstrates that overexpression of eNOS protein causes a marked increase in neocapillary formation in response to tissue ischemia without affecting ischemia-induced VEGF expression or VEGF-mediated Akt phosphorylation.
京府医大 Previous studies reported that VEGF stimulates the release of NO from the arterial wall and promotes the recovery of disturbed endothelium-dependent flow in the ischemic hindlimb.
関西医大 In vitro studies demonstrated that VEGF stimulates the release of NO from the normal arterial wall and promotes the recovery of disturbed endothelium-dependent flow in the rabbit ischemic hindlimb.
京府医大 Direct in vitro evidence that NO may induce angiogenesis was demonstrated recently by Papapetropoulos et al. Ziche et al established the first line of evidence that NO can induce angiogenesis in vitro. Murohara et al clearly showedNO-mediated angiogenesis in response to tissue ischemia in NO-deficient mice.
関西医大 Direct in vitro evidence that NO may induce angiogenesis was demonstrated recently by Papapetropoulos et al. Ziche et al established the first line of evidence that NO can induce angiogenesis in vitro. Murohara et al clearly showed NO-mediated angiogenesis in response to tissue ischemia by using NO-deficient mice.
両論文とも責任著者は同一人物のようです。
次回でこのシリーズ最終回となります。
超一流雑誌の論文が登場します。
Retraction Watch / 2011.07.04 00:03 / 推薦数 : 15
このシリーズは今回で最終回となります。
ランセットに掲載された解説論文を紹介します。
著者はひとりのみで2004年の発表。
すでに舞台は京都府立医大に移っています。
ランセット論文 Haemopoietic stem cells that give rise to blood cells and which move between bone marrow and peripheral blood are the best characterised adult stem cells in man. Recent data suggest that adult stem cells generate differentiated cells of a different cell type beyond their own tissue boundaries, a process termed “developmental plasticity”.
Various stem-cell preparations originating from haemopoietic tissue have been used in in-vivo studies of stem-cell plasticity, including unselected cells from bone marrow, purified haemopoietic stem cells, and single haemopoietic stem cells that originate from either bone marrow or peripheral blood.
別の論文A Hematopoietic stem cells that give rise to blood cells and move between bone marrow and peripheral blood are the best-characterized adult stem cells in humans. Recent data suggest that adult stem cells generate differentiated cells beyond their own tissue boundaries, a process termed ‘developmental plasticity.’
Various stem-cell preparations originating from hematopoietic tissue have been used in in vivo studies of stem-cell plasticity, including unselected cells from bone marrow, purified hematopoietic stem cells, and single hematopoietic stem cells that originate from either bone marrow or peripheral blood.
ランセット論文 Acute myocardial infarction is the most common cause of morbidity and mortality in more developed countries. Therapeutic advances have mainly been targeted at restoring antegrade perfusion in the infarct-related artery.
別の論文B Acute myocardial infarction is the most common cause of morbidity and mortality in more developed countries. Therapeutic advances have mainly been targeted at restoring antegrade perfusion in the infarct-related artery,
ランセット論文 Despite rapid restoration of perfusion, postinfarction heart failure remains a major challenge.A substantial step forward in reversing abnormal cardiac remodelling would be the enhanced generation of cardiac myocytes as well as the stimulation of neovascularisation within the infarcted area.
別の論文C However, despite rapid restoration of blood flow, postinfarction heart failure remains a major challenge.The major goal to reverse LV remodeling would be the enhancement of regeneration of cardiac myocytes as well as the stimulation of neovascularization within the infarct area
別の論文A,B,C ともランセット論文より先に公開されています。
ランセット論文の著者は論文A,B,C の著者ではありません。
原著論文が掲載され、それにともなって解説論文が加わることは、その原著論文の著者らにとっては、大変名誉なことです。
しかし、このような形で自分の論文が解説されると、喜んでいいのかどうか、 悩んでしまうところです。
2003年という年をよく覚えておいて下さいと、シリーズの一番最初にお願いしました。なぜだかわかりますか？
平成15年（２００3年）4月に京都府立医科大学は大学院大学に再編され、内科学第二講座は、循環器内科学、腎臓・高血圧内科学、呼吸器内科学の3部門に分化しました。私が平成15年（２００3年）4月1日より初代の循環器内科学教授に就任しました。
なのだそうです。
撤回された時にはすでに就任していたのでしょうか？
微妙なところです。
