Retraction Watch

Tracking retractions as a window into the scientific process

Déjà vu: JBC epigenetics paper is retracted, then largely re-published with fewer authors

with 9 comments

JBCA group of authors have withdrawn a 2011 Journal of Biological Chemistry paper, but then appear to have re-published almost the same paper a month later, only this time with just five of the original nine authors.

The paper, “HDAC3-dependent reversible lysine acetylation of cardiac myosin heavy chain isoforms modulates their enzymatic and motor activity,” concerns a type of protein regulation important to cardiac stress. Written by researchers at the University of Chicago and the University of Pittsburgh, it has been cited 16 times, according to Thomson Scientific’s Web of Knowledge. It was rated “Exceptional” by a reviewer on the Faculty of 1000 website.

As we’ve come to expect from the JBC, here’s the full retraction notice, in all its inexplicit glory:

This article has been withdrawn by the authors.

Here’s where it gets strange: As far as we can tell, the 2011 paper was retracted in March, but then re-published, with the same title and almost exact same text, in April.

The single major difference we can find between the two papers is that the 2015 version leaves out four of the 2011 authors: David S. Courson, Minjia Tan, Yingming Zhao, and Ronald S. Rock, all of the University of Chicago.

For an example of the similarity between the two papers, here’s the abstract of the retracted December 21, 2010 paper:

Reversible lysine acetylation is a widespread post-translational modification controlling the activity of proteins in different subcellular compartments. We previously demonstrated that a class II histone deacetylase (HDAC), HDAC4, and a histone acetyltransferase, PCAF, associate with cardiac sarcomeres, and a class I and II HDAC inhibitor, trichostatin A, enhances contractile activity of myofilaments. In this study, we show that a class I HDAC, HDAC3, is also present at cardiac sarcomeres. By immunohistochemical and electron microscopic analyses, we found that HDAC3 was localized to the A band of sarcomeres and was capable of deacetylating myosin heavy chain (MHC) isoforms. The motor domains of both cardiac – and -MHC isoforms were found to be reversibly acetylated. Biomechanical studies revealed that lysine acetylation significantly decreased the Km for the actin-activated ATPase activity of both – and -MHC isoforms. By an in vitro motility assay, we found that lysine acetylation increased the actin sliding velocity of -myosin by 20% and -myosin by 36%, compared to their respective non-acetylated isoforms. Moreover, myosin acetylation was found to be sensitive to cardiac stress. During induction of hypertrophy, myosin isoform acetylation increased progressively with duration of stress stimuli, independent of isoform shift, suggesting that lysine acetylation of myosin could be an early response of myofilaments to increase contractile performance of the heart. These studies provide the first evidence for localization of HDAC3 at myofilaments and uncover a novel mechanism modulating the motor activity of cardiac MHC isoforms.

And here’s the abstract of the April 24, 2015 paper. The differences, which we’ve highlighted in bold, are only cosmetic:

Reversible lysine acetylation is a widespread post-translational modification controlling the activity of proteins in different sub-cellular compartments. We previously demonstrated that a classII HDAC, HDAC4 and a HAT, PCAF associate with cardiac sarcomeres, and a class-I and -II HDAC inhibitor, trichostatin A, enhances contractile activity of myofilaments. In this study we show that a class-I HDAC, HDAC3 is also present at cardiac sarcomeres. By immuno-histochemical and electron microscopic analyses we found that HDAC3 was localized to Aband of sarcomeres, and was capable of deacetylating myosin heavy chain (MHC) isoforms. The motor domains of both cardiac α- and β-MHC isoforms were found to be reversibly acetylated. Biomechanical studies revealed that lysine acetylation significantly decreased the Km for the actin-activated ATPase activity of MHC isoforms. By in vitro motility assay we found that lysine acetylation increased the actin-sliding velocity of α-myosin by 20% and β-myosin by 36%, compared to their respective non-acetylated isoforms. Moreover, myosin acetylation was found to be sensitive to cardiac stress. During induction of hypertrophy, myosin isoform acetylation increased progressively with duration of stress-stimuli, independent of isoform shift, suggesting that lysine acetylation of myosin could be an early response of myofilaments to increase contractile performance of the heart. These studies provide first evidence for localization of HDAC3 at myofilaments and uncover a novel mechanism modulating the motor activity of cardiac MHC isoforms.

We asked the JBC to explain what happened. Karou Sakabe, manager of publication issues at the American Society for Biochemistry and Molecular Biology, the publisher of the JBC, wrote:

It is JBC policy to maintain confidentiality in such matters.  Please direct your inquiry to Dr. Gupta.

We should note that although this is what we’ve come to expect from the JBC, it’s nonetheless disappointing that they continue to squander an opportunity. In 2012, the ASBMB created a new position, “manager of publication ethics,” with a job description that included “Write and/or help authors write corrections and retractions.” We were hopeful that it would lead to appropriately detailed retraction notices, but with rare exception, that has not been the case. (The position no longer appears on their staff list, but Sakabe’s role would appear to have taken its place. ) We recognize that opaque notices aren’t the fault of the person in that job, but of senior ASBMB management who stubbornly stick to policies that aren’t good for science.

In any case, we have repeatedly reached out to corresponding author Mahesh P. Gupta (the last author on both versions) and co-author of paper #1 Ronald Rock in the hopes of more information. We’ll update if we hear back.

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Written by Megan Scudellari

May 13th, 2015 at 11:30 am

Comments
  • Leonid Schneider May 13, 2015 at 12:23 pm

    Weird indeed. Let us assume that it was indeed the only issue with some authorships wrongly assigned. This could have been easily rectified by a correction. Another JBC mystery…

  • oldnuke May 13, 2015 at 12:53 pm

    So is Rock playing Scissors and Papers? 🙂

  • Dave May 14, 2015 at 10:30 am

    JBC is stuck in a time when people actually thought it was a good journal. Their arrogance when it comes to issues of misconduct/retractions is ridiculous. No wonder their IF is still taking a nosedive with this kind of management

  • Paul Brookes May 14, 2015 at 11:53 am

    From the same lab, originally reported on a certain blog in 2012…
    Am J Physiol Heart Circ Physiol 294: H1388–H1397, 2008 (PMID 18192211)
    http://imgur.com/7t6oGVY
    http://imgur.com/qLW9ivb
    Also tagged independently on PubPeer, not by me (https://pubpeer.com/publications/18192211)

  • fernandopessoa October 26, 2015 at 2:36 pm

    Another Mahesh P Gupta paper under scrutiny at Pubpeer.

    https://pubpeer.com/publications/65A10C69BA4146AF84F77063FA6785#fb39354

  • fernandopessoa October 26, 2015 at 3:03 pm

    Another Mahesh P Gupta publication under scrutiny at Pubpeer.

    https://pubpeer.com/publications/9819411

  • fernandopessoa October 28, 2015 at 5:22 am

    Another Mahesh P Gupta publication under scrutiny at Pubpeer.

    https://pubpeer.com/publications/579B412DEA6340E9520A5E9744E920#fb39398

  • fernandopessoa March 24, 2017 at 7:03 am

    Two 2017 retractions for Mahesh P Gupta.

    1. J Biol Chem. 2013 Apr 19;288(16):11216-32. doi: 10.1074/jbc.M112.442384. Epub 2013 Feb 27.
    A cardiac-enriched microRNA, miR-378, blocks cardiac hypertrophy by targeting Ras signaling.

    Nagalingam RS1, Sundaresan NR, Gupta MP, Geenen DL, Solaro RJ, Gupta M.
    Author information
    1
    Department of Physiology and Biophysics and Center for Cardiovascular Research, University of Illinois, Chicago, Illinois 60612, USA.

    2017 retraction notice.
    http://www.jbc.org/content/292/12/5123

    VOLUME 288 (2013) PAGES 11216–11232

    This article has been withdrawn by the authors. Lanes 1 and 2 of the actin immunoblot in Fig. 3B were reused in lanes 3 and 4 of the actin immunoblot in Fig. 7C. The ANF immunoblot in Fig. 3B was reused as ANF in Fig. 9F. Control lanes 1 and 2 of the ANF immunoblot in Fig. 8C were duplicated. The Grb2 and GAPDH immunoblots in Fig. 9C were inappropriately manipulated.

    © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

    2. J Biol Chem. 2014 Sep 26;289(39):27199-214. doi: 10.1074/jbc.M114.580977. Epub 2014 Aug 7.
    Deficiency of cardiomyocyte-specific microRNA-378 contributes to the development of cardiac fibrosis involving a transforming growth factor β (TGFβ1)-dependent paracrine mechanism.

    Nagalingam RS1, Sundaresan NR2, Noor M1, Gupta MP2, Solaro RJ1, Gupta M3.
    Author information
    1
    From the Department of Physiology and Biophysics and Center for Cardiovascular Research, University of Illinois, Chicago, Illinois 60612 and.
    2
    the Department of Cardiothoracic Surgery, University of Chicago, Chicago, Illinois 60637.
    3
    From the Department of Physiology and Biophysics and Center for Cardiovascular Research, University of Illinois, Chicago, Illinois 60612

    2017 retraction notice.
    http://www.jbc.org/content/292/12/5124

    VOLUME 289 (2014) PAGES 27199–27214

    This article has been withdrawn by the authors due to reuse of the U6 loading controls in the right and left panels of Fig. 4A and the GAPDH loading controls in Figs. 7D and 9F. Additionally, the journal investigated the IGF1R immunoblot in Fig. 5C and the collagen immunoblot in Fig. 6C. The authors were not able to provide the original data for the collagen immunoblot in Fig. 6C.

    © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

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