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.
Figure 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.
Format: JPEG Size: 37KB Download file
References
-
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
