A team of neuroscientists in Japan has lost their 2012 article in Brain Research for duplicating elements of a figure from a paper they’d published earlier that year in another journal.
The article, “Dynamic changes of mitochondrial fission proteins after transient cerebral ischemia in mice,” came from a lab at Okayama University. The last author was Koji Abe. According to the retraction notice:
This article has been retracted at the request of the corresponding Author owing to the inadvertent duplication of some data [p-Drp-1 blots presented in fig. 2] between this article and “Dynamic changes of mitochondrial fusion and fission proteins after transient cerebral ischemia in mice”, Liu, W, Tian, F, Kurata, T, Morimoto, N, Abe, K. J. Neurosci. Res., 90 (6) (2012) 1183–1189, http://dx.doi.org/10.1002/jnr.23016.
We thought the titles of the two papers were awfully close for comfort, and, while the articles do seem to overlap quite a bit, they’re not identical.
Here’s the abstract from the Brain Research paper:
With fusion or fission, mitochondria alter their morphology in response to various physiological and pathological stimuli resulting in either elongated, tubular, interconnected or fragmented form. Immunohistochemistry and Western blot analyses were performed at 2, 7, 14 and 28 d after 90 min of transient middle cerebral artery occlusion (tMCAO) in mice. The present study showed that mitochondrial fission protein fission 1 (Fis1) and phosphorylated dynamin-related protein 1 (P-Drp1) both progressively increased with the peak at 14 d after tMCAO. Double immunofluorescent analysis showed the number of double positive cells with Fis1/Drp1 reduced between 2 and 28 d after 90 min of tMCAO, and also showed some double positive cells with Fis1/terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) in the peri-infract regions at 2d after the reperfusion. The present study suggests a progressive activation of mitochondrial fission proteins Fis1 and P-Drp1 in relation to apoptotic process in neural cells of the peri-infract regions after tMCAO.
And the one from the Journal of Neuroscience Research:
With fusion or fission, mitochondria alter their morphology in response to various physiological and pathological stimuli, resulting in elongated, tubular, interconnected, or fragmented forms. Immunohistochemistry and Western blot analysis were performed at 2 days, 7 days, 14 days, and 28 days after 90 min of transient middle cerebral artery occlusion (tMCAO) in mice. This study showed that mitochondrial fission protein dynamin-related protein 1 (Drp1) and fusion protein optic atrophy 1 (Opa1) were both upregulated in the ischemic penumbra, with the peak at 2 days after tMCAO, whereas phosphorylated-Drp1 (P-Drp1) progressively increased with a peak at 14 days after tMCAO. Double-immunofluorescence analysis showed many Drp1/cytochrome c oxidase subunit l (COX1) double-positive cells and Opa1/COX1 double-positive cells in the ischemic penumbra and also showed some double-positive cells with Drp1/terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) and Opa1/TUNEL in the ischemic penumbra. In contrast, both Drp1 and Opa1 showed progressive decreases until 2 days after tMCAO in the ischemic core because of necrotic brain damage. The present study suggests that there was a continuous mitochondrial fission and fusion during these periods in the ischemic penumbra after tMCAO, probably in an effort toward mitophagy and cellular survival.
So, same study design (and quite possibly the same experiment) but different proteins.