Cardiovascular Research has retracted a 2010 paper by a group of prominent cardiology researchers in Brazil.
The reason: Image manipulation — which the authors say didn’t materially affect the conclusions of the paper.
The article, “FAK mediates the activation of cardiac fibroblasts induced by mechanical stress through regulation of the mTOR complex,” came from a group led by Ana Paula Dalla Costa, from the State University of Campinas.
Here’s the abstract of the study, which has been cited 19 times, according to Thomson Scientific’s Web of Knowledge:
AIMS:
Cardiac fibroblasts are activated by mechanical stress, but the underlying mechanisms involved remain poorly understood. In this study, we investigated whether focal adhesion kinase (FAK) plays a role in the activation of cardiac fibroblasts in response to cyclic stretch.
METHODS AND RESULTS:
Neonatal (NF-P3/80–third passage, 80% confluence) and adult (AF-P1/80–first passage, 80% confluence) rat cardiac fibroblasts were exposed to cyclic stretch (biaxial, 1 Hz), which enhanced FAK phosphorylation at Tyr397. Proliferation (anti-5-bromo-2′-deoxyuridine and anti-Ki67 nuclear labelling), differentiation into myofibroblasts (expression of alpha-smooth muscle actin–alpha-SMA), and the activity of matrix metalloproteinase-2 were equally enhanced in stretched NF-P3/80 and AF-P1/80. Treatment with the integrin inhibitor RGD peptide impaired FAK phosphorylation and increased apoptosis (TUNEL) in non-stretched and stretched NF-P3/80, whereas FAK silencing induced by small interfering RNA modestly enhanced apoptosis only in stretched cells. RGD peptide or FAK silencing suppressed the activation of NF-P3/80 invoked by cyclic stretch. In addition, NF-P3/80 depleted of FAK were defective in AKT Ser473, TSC-2 Thr1462, and S6 kinase Thr389 phosphorylation induced by cyclic stretch. The activation of NF-P3/80 invoked by cyclic stretch was prevented by pre-treatment with the mammalian target of rapamycin (mTOR) inhibitor rapamycin, whereas supplementation with the amino acid, leucine, activated S6K and rescued the stretch-induced activation of NF-P3/80 depleted of FAK.
CONCLUSIONS:
These findings demonstrate a critical role for the mTOR complex, downstream from FAK, in mediating the activation of cardiac fibroblasts in response to mechanical stress.
But as the notice explains:
The study by Dalla Costa et al. reported an analysis of the role of focal adhesion kinase in the activation of cardiac fibroblasts in response to mechanical stress. The senior author recently identified errors affecting several figure panels where the loading controls for Western blots are duplicated presentations of the same gels. The first author has acknowledged responsibility for the preparation of the figures for publication. While the senior author confirms the reproducibility of the experimental data and the validity of the conclusions, the figures in the manuscript by Dalla Costa et al. compromise the current manuscript warranting retraction. The authors apologize for the disturbance this may have caused.
We couldn’t find any other retractions from this group so far. But we did find a blot-related correction from earlier this year. The article, “MEF2C Silencing Attenuates Load-Induced Left Ventricular Hypertrophy by Modulating mTOR/S6K Pathway in Mice,” in PLoS One, did not include Dalla Costa, although the senior author again is Kleber Franchini. Here’s the notice:
Figure 3 is incorrect. The Western blot in Figure 3c should have four bands instead of five. The authors have provided a corrected version of Figure 3 here.
The notice states: “The senior author recently identified errors affecting several figure panels […]”, but perhaps a more accurate sentence would be: “The senior author has been warned recently, via a PubPeer post, of errors affecting several figure panels […]”.
“The senior author recently identified errors affecting several figure panels where the loading controls for Western blots are duplicated presentations of the same gels.”
Only if senior author decided to contact PubPeer anonymously before requesting the retraction.
https://pubpeer.com/publications/674EC59B787FD43F30F87307D97F20
Journal editors and authors usually pretend PubPeer doesn’t exist, even when it was the cause of their actions. Yet, alas, indeed acknowledging PubPeer would expose several other reported apparent issues in the retracted paper.
If the data is reproducible and the paper’s conclusions valid why did they choose to retract rather than simply repeat the westerns (with the proper controls) and post a correction?
After looking at the link CR provided I think I have my answer.
It is interesting to note that according with new rules from funding agencies, any (self-)allegation of fraud in Science in Brazil is eligible to official investigation and sanctions to PIs. Thus today, more than ever, retraction notices from Brazilian authors must make it officially clear that PIs never knew about any issue, had no intention behind whatever is found, and that these do not affect their work significantly. In face of evident manipulation or plagiarism these official statements can be quite amusing, though rather sad.
The journal and its editor need to be applauded. This is a decision big enough to cause a heart attack in any researcher, but what goes around, comes around. And for such a small reason, like a little clot in the artery. So, how can we get such rigorous post-publication integrity from other publishers and journals? Perhaps this is one way. By having sufficient examples will allow the public to then add pressure on other journals and publishers to pull equally problematic papers from their journals, or face serious public shame. Like it or not, I think the publishers are going to start breaking out int a serious sweat pretty soon, if they haven’t started to sweat already as they realize how their traditional peer review model has failed and eluded them. I predict that 2015 will see a massive spike in academic claims, and perhaps a peak in retractions, as the camel’s back starts to break, and its heart stops to pump. We have the responsibility of lending support to PubPeer, PubMed Commons, RW, Beall’s blog, The Scholarly Kitchen and other rising blogs in science-related tpics because it is ultimately the voices of the masses that will have to reign control back from the publishers and show the way that science publishing needs to progress. This, even though we may share differences of opinion, or strategy.
I don’t think SK is the place to be looking for that.
While the senior author confirms the reproducibility of the experimental data and the validity of the conclusions
These boiler-plate self-exculpatory statements from senior authors are all very well, but they leave you wondering, how is the senior author in a position to confirm anything if he pays so little attention to the papers he signs his name to?
I disagree, Narad. The Scholarly Kitchen provides a very different set of analyses about aspects of the world of publishing that is absolutely valuable for researchers. There is alot of valuable information and opinion on that site. I do admit that that site is very protective of the publishers in many instances, probably given the massive link that many of the writers on that blog have with commercial publishers. But that is not always a bad thing, because it gives us “insider” perspectives. The comment section is excessively moderated, admittedly, and analyses of errors in papers is not possible, or appropriate, but that site is valuable, nonetheless.
JATdS, regarding SK, my comment was in reference to your suggestion that it was a site that has some bearing on reining in the failings of the status quo. (I did not get the impression that you meant it as an example of entrenchment.) A general rant would be off-topic, but I will tempt fate by noting that these are folks who think that the uncurated mess that is CrossRef represents a ground-breaking technological innovation.
I would call this an understatement, but similarly, I would call to your attention their take on (“acceptable”) PPPR.
JATdS, SK is a blog of the Society for Scholarly Publishing. It does look to me like a organisation that is quite heavily influenced by commercial publishers. It might be interesting to see their point of view, but that’s about it IMHO.
Duplications?? Really??
http://i.imgur.com/XY34upP.png
These figures from other articles are also interesting:
1)Circulation Research (2007)
http://i.imgur.com/R1fSHQm.png
2) Nat Commun, 5 (2014)
http://i.imgur.com/E3omVX8.png
3)Am. J. Physiol. Regul. Integr. Comp. Physiol., 289 (2005)
http://i.imgur.com/w48Z3fn.png
In fairness, SK sort of disavows representing the SSP itself.