Correction: Transcriptomics and proteomics analyses of the PACAP38 influenced ischemic brain in permanent middle cerebral artery occlusion model mice

  • Motohide Hori1, 2,

    Affiliated with

    • Tomoya Nakamachi2, 3,

      Affiliated with

      • Randeep Rakwal2, 4Email author,

        Affiliated with

        • Junko Shibato2,

          Affiliated with

          • Tetsuo Ogawa2,

            Affiliated with

            • Toshihiro Aiuchi2,

              Affiliated with

              • Tatsuaki Tsuruyama1,

                Affiliated with

                • Keiji Tamaki1 and

                  Affiliated with

                  • Seiji Shioda2Email author

                    Affiliated with

                    Journal of Neuroinflammation201310:18

                    DOI: 10.1186/1742-2094-10-18

                    Received: 31 January 2013

                    Accepted: 31 January 2013

                    Published: 31 January 2013

                    The Figure Two (Figure 1 here), X-axis description of each sample was inverted in the original publication [1].
                    http://static-content.springer.com/image/art%3A10.1186%2F1742-2094-10-18/MediaObjects/12974_2013_791_Fig1_HTML.jpg
                    Figure 1

                    The mRNA expression profiles of differentially expressed genes. Both the upregulated (A) and downregulated (B) genes were selected randomly. Gel images on top show the polymerase chain reaction (PCR) product bands stained with ethidium bromide; the band intensities are also presented graphically below for clarity. Lane numbers 1 to 8 indicate sham control (lanes 1, 2, 5, and 6) and permanent middle cerebral artery occlusion (PMCAO) treatment (lanes 3, 4, 7, and 8), respectively. P indicates pituitary adenylate cyclase-activating polypeptide (PACAP) treatment; C is the control (minus PACAP). GAPDH and beta-actin genes were used a positive control (C). Semi-quantitative RT-PCR was performed as described in Methods, and the specific 3’-UTR primers are detailed in Additional file 2: Table S2.

                    With reference to corrected Figure Two (Figure 1 here), we have the following revised text.

                    On Page 9, left column: lines 19-24 should read as -

                    “Similarly, Il6, S100a5, Il22, Il1b, Igf1, and Ccl2 were highly expressed at 6 h in the PACAP-treated ischemic brain, whereas their expression level decreased at 24 h compared to the PMCAO effect alone (Figure Two (Figure 1 here)). Fgf21, Pitpnc1, and Epha3 genes showed an increase in expression at 24 h over PMCAO alone (Figure Two (Figure 1 here)).”

                    On Page 11, right column: lines 16-19 should read as -

                    “In the ischemic hemisphere at 24 h, the PACAP plus PMCAO expression level of Il6 was also reduced compared to the PMCAO plus saline control.”

                    We regret any inconvenience that this inaccuracy in Figure Two (Figure 1 here) and therein the figure legend, which could not be properly corrected at the proof stage, in the originally published manuscript might have caused.

                    Authors’ Affiliations

                    (1)
                    Department of Forensic Medicine and Molecular Pathology, School of Medicine, Kyoto University
                    (2)
                    Department of Anatomy I, School of Medicine, Showa University
                    (3)
                    Department of Center for Biotechnology, Showa University
                    (4)
                    Graduate School of Life and Environmental Sciences, University of Tsukuba

                    References

                    1. Hori M, Nakamachi T, Rakwal R, Shibato J, Ogawa T, Aiuchi T, Tsuruyama T, Tamaki K, Shioda S: Transcriptomics and proteomics analyses of the PACAP38 influenced ischemic brain in permanent middle cerebral artery occlusion model mice. J Neuroinflammation 2012, 9:256.PubMedView Article

                    Copyright

                    © Hori et al.; licensee BioMed Central Ltd. 2013

                    This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://​creativecommons.​org/​licenses/​by/​2.​0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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