Abstract
To gain additional insights into the pathogenic cellular and molecular mechanisms underlying different types of brain injury (e.g., trauma versus ischemia), recently attention has focused on the discovery and study of protein biomarkers. In previous studies, using a high-throughput immunoblotting (HTPI) technique, we reported changes in 29 out of 998 proteins following acute injuries to the rat brain (penetrating traumatic versus focal ischemic). Importantly, we discovered that one protein, endothelial monocyte-activating polypeptide II precursor (p43/pro-EMAPII), was differentially expressed between these two types of brain injury. Among other functions, p43/pro-EMAPII is a known pro-inflammatory cytokine involved in the progression of apoptotic cell death. Our current objective was to verify the changes in p43/pro-EMAPII expression, and to evaluate the potentially important implications that the differential regulation of this protein has on injury development. At multiple time points following either a penetrating ballistic-like brain injury (PBBI), or a transient middle cerebral artery occlusion (MCAo) brain injury, tissue samples (6–72 h), CSF samples (24 h), and blood samples (24 h) were collected from rats for analysis. Changes in protein expression were assessed by Western blot analysis and immunohistochemistry. Our results indicated that p43/pro-EMAPII was significantly increased in brain tissues, CSF, and plasma following PBBI, but decreased after MCAo injury compared to their respective sham control samples. This differential expression of p43/pro-EMAPII may be a useful injury-specific biomarker associated with the underlying pathologies of traumatic versus ischemic brain injury, and provide valuable information for directing injury-specific therapeutics.
Expression of Concern:
Readers are advised that after receiving an alert regarding a comment on the PubPeer platform,1 the Journal of Neurotrauma attempted to contact the authors of a paper published in 2009 entitled, “P43/pro-EMAPII: A Potential Biomarker for Discriminating Traumatic Versus Ischemic Brain Injury,” by Changping Yao, Anthony J. Williams, Andrew K. Ottens, X.-C. May Lu, Ming Cheng Liu, Ronald L. Hayes, Kevin K. Wang, Frank C. Tortella, and Jitendra R. Dave (J Neurotrauma. 2009:26(8):1295-1305.; doi: 10.1089/neu.2008.0811), requesting information and/or clarification on the post which claimed possible figure duplication.
After receiving the alert, independent analyses run by the journal confirmed a duplicated panel in Figure 5: M-C 24 and 72 hours, as well as a potential duplication with panels M-C and M-I.
One of the co-authors, Dr. Kevin Wang, replied1 directly on the PubPeer platform, indicating:
“I agree with you that the control shown as 72 h and at 24 h are likely the same.
The data were generated not by our team by at WRIAR, I know that senior author Dr. Dave also passed away many years ago now.
If so, it was likely duplicated during image sorting inadvertently.
Hope this is helpful.”
Journal of Neurotrauma
issues this Expression of Concern for readers to take this into consideration.
1. Actinopolyspora biskrensis.
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