In the above article [Mugabe BE, Yaghini FA, Song CY, Buharalioglu CK, Waters CM, and Malik KU (2010) J Pharmacol Exp Ther 332:116–124], a reader raised the question regarding the data in Fig. 8, which shows that the c-Src inhibitor PP2 abolished the wound healing of vascular smooth muscle cells (VSMCs) and phosphorylation of the epidermal growth factor receptor (EGFR) elicited by epidermal growth factor (EGF). Given that EGF does not cause c-Src phosphorylation, one would expect that it should not alter EGF-induced cell migration and EGFR phosphorylation unless PP2 has some nonspecific effect on EGF-induced VSMC migration and EGFR phosphorylation. Unfortunately, these data escaped attention of the authors, and the discrepancy in the article was not discovered prior to its publication.
After reviewing all of the data, the authors discovered an error in the analysis of the effect of PP2 on EGF-induced wound healing and EGFR phosphorylation. Additional experiments were conducted to examine the effect of the c-Src inhibitor PP2 on Ang II- and EGF-induced VSMC migration and EGFR phosphorylation. These experiments confirmed the authors' original observation that PP2 inhibits Ang II-induced VSMC migration and phosphorylation of EGFR, c-Src, and extracellular signal-regulated kinase 1/2 but not p38 mitogen-activated protein kinase (Fig. 3 in the original article); however, the authors neglected to observe an inhibitory effect of PP2 on EGF-induced VSMC migration and on the basal or EGF-induced EGFR phosphorylation, although previous data on the lack of effect of EGF and PP2 on c-Src phosphorylation and that of PP2 on EGF-induced ERK1/2 and p38 MAPK phosphorylation were confirmed as shown in Fig. 8 of the original article. The data from the new experiments are shown in the revised version of Fig. 8 in the online version of the corrected article. The revised figure shows the lack of inhibitory effect of PP2 on EGF-induced VSMC migration and EGFR phosphorylation. Moreover, the authors have confirmed these observations by performing additional series of experiments by using small interfering Src RNA and dominant negative Src mutant containing adenoviruses (Figs. 1 and 2 here; also available as Supplemental Data online).
The online versions of the article and table of contents will be corrected in departure from the print version.
The authors regret these errors and apologize for any confusion or inconvenience they may have caused.
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