Correction

Correction: mPGES-1 null mice are resistant to bleomycin-induced skin fibrosis

Matthew R McCann1, Roxana Monemdjou2, Parisa Ghassemi-Kakroodi1, Hassan Fahmi1, Gemma Perez2, Shangxi Liu1, Xu Shi-wen3, Sunil K Parapuram1, Fumiaki Kojima4, Christopher P Denton3, David J Abraham3, Johanne Martel-Pelletier2, Leslie J Crofford4, Andrew Leask1 and Mohit Kapoor2*

Author Affiliations

1 The Canadian Institute of Health Research Group in Skeletal Development and Remodeling, Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London, Ontario, N6A 5C1, Canada

2 Osteoarthritis Research Unit, University of Montreal Hospital Research Center (CR-CHUM) and Department of Medicine, University of Montreal, 1560 Rue Sherbrooke Est, Montréal, Québec, H2L 4M1, Canada

3 Centre for Rheumatology, Department of Medicine, University College London (Royal Free Campus), Rowland Hill Street, London, NW3 2PF, UK

4 Division of Rheumatology, Department of Internal Medicine, University of Kentucky, 740 S. Limestone Street, J-509 Kentucky Clinic, Lexington, KY 40536, USA

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Arthritis Research & Therapy 2011, 13:402  doi:10.1186/ar3285


See related research article by McCann et al., http://arthritis-research.com/content/13/1/R6


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/13/2/402


Published:24 March 2011

© 2011 BioMed Central Ltd

Correction

Following publication of our recent article [1], an error in Figure 5d was noticed. In Figure 5d, the β-actin blot corresponding to α-SMA blot was captured on the chemiluminescence imaging system in an inverted orientation. Since this imager does not capture the protein marker, an error in the orientation of the membrane while capturing the picture of the blot occurred. During preparation of the figures for Figure 5d, the α-SMA blot was in right orientation but since orientation of β-actin blot was inverse as it was captured inversely resulted in non-corresponding β-actin blot with respect to α-SMA blot. We have rectified this error now and β-actin blot now corresponds to α-SMA blot. The corrected figure 5 is given here as Figure 1 and a supplementary figure 1 (Additional file 1) showing another set of blots representing Figure 5d is also provided.

thumbnailFigure 1. mPGES-1 genetic deletion results in reduced collagen content and myofibroblast formation in vivo. (a) Hydroxyproline analysis showed reduced collagen content in mPGES-1 null mice compared with wild-type (WT) mice in response to bleomycin treatment. Data from four separate mice per group are shown. (b, c) Immunohistochemistry using anti-α-SMA antibody was performed. mPGES-1 null mice showed a reduced number of α-SMA-expressing myofibroblasts compared with WT mice in response to bleomycin treatment (4-week treatment). Representative data from four separate animals per group are shown. *P < 0.05; bleomycin-treated WT and mPGES-1 null mice compared with phosphate-buffered saline (PBS)-treated mice. +P < 0.05; bleomycin-treated mPGES-1 null mice compared with bleomycin-treated WT mice. (d) Protein extracts from skin tissue after 4 weeks of bleomycin or PBS treatment were subjected to Western blot analysis with an anti-α-SMA antibody. mPGES-1 null mice treated with bleomycin showed reduced α-SMA expression compared with bleomycin-treated WT mice. Representative blot from four separate animals per group is shown. α-SMA, alpha-smooth muscle actin; mPGES-1, microsomal prostaglandin E2 synthase-1.

Additional file 1. Supplementary Figure 1. mPGES-1 genetic deletion results in reduced α-SMA expression in response to bleomycin treatment. Protein extracts from skin tissue after 4 weeks of bleomycin or PBS treatment were subjected to Western blot analysis with an anti-α-SMA antibody. mPGES-1 null mice treated with bleomycin showed reduced α-SMA expression compared with bleomycin-treated WT mice. Representative blot from four separate animals/group/genotype is shown. (b) Graph represents α-SMA expression normalized to β-actin expression from four separate animals/group/genotype. *P < 0.05; bleomycin-treated WT and mPGES-1 null mice compared with PBS-treated mice. +P < 0.05; bleomycin-treated mPGES-1 null mice compared with bleomycin-treated WT mice. α-SMA, alpha-smooth muscle actin; β-actin, beta-actin; mPGES-1, microsomal prostaglandin E2 synthase-1.

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References

  1. McCann MR, Monemdjou R, Fahmi H, Perez G, Liu S, Shi-wen X, Parapuram SK, Kojima F, Denton CP, Abraham DJ, Martel-Pelletier J, Crofford LJ, Leask A, Kapoor M: mPGES-1 null mice are resistant to bleomycin-induced skin fibrosis.

    Arthritis Res Ther 2011, 13:R6. PubMed Abstract | BioMed Central Full Text OpenURL