Correction: Corrigendum: Angiotensin II type 1 receptor blockade attenuates TGF-β–induced failure of muscle regeneration in multiple myopathic states

Nat. Med. 12, 204–210 (2007); published online 21 January 2007; corrected after print 27 February 2007

In the version of this article initially published, the same panels were inadvertently used to show negative pSmad2/3 and periostin staining in muscle of Fbn1^C1039G/+ mice treated with TGF-β–neutralizing antibody in both the steady-state (Fig. 1a, right column, second and third rows, respectively) and muscle-regeneration (Fig. 1b, right column, third and fourth rows, respectively) experiments. In reality, these images only relate to the steady-state experiment (Fig. 1a). The intended images for Figure 1b are provided (red, pSmad2/3 staining; green, periostin staining). As both sets of images show negative staining in neutralizing antibody–treated Fbn1^C1039G/+ mice, this does not alter any observations or conclusions discussed in the manuscript. The error has been corrected in the HTML and PDF versions of the article.

Figure 1: Evaluation of steady-state and regenerating skeletal muscles in fibrillin-1 deficient mice.

(a) Hematoxylin and eosin staining of quadriceps muscle (upper panels) shows marked variation of fiber size in Fbn1^C1039G/+ mice. Note several small and split fibers (asterisks), fibers with central nucleation and endomysial thickening. TGF-β antagonism in vivo reverses myopathic architecture in Fbn1^C1039G/+ mice. Increased TGF-β signaling, as evidenced by nuclear accumulation of pSmad2/3 (middle panels) and periostin expression (lower panels) in Fbn1^C1039G/+ mice, when compared to wild-type mice or Fbn1^C1039G/+ mice treated with TGF-β–neutralizing antibody. Analysis of the cross-sectional area (myofiber CSA in μm²) of tibialis anterior muscle fibers shows a decrease in fiber size in Fbn1^C1039G/+ mice when compared to wild-type mice or Fbn1^C1039G/+ mice treated with TGF-β–neutralizing antibody (graph). Scale bars, 70 μm (low magnification) and 50 μm (high magnification, inset boxes). (b) Impaired muscle regeneration in Fbn1^C1039G/+ mice. Few newly-formed muscle fibers and disorganized muscle architecture with numerous small fibers (arrows) 4 and 18 days after cardiotoxin-induced muscle injury, respectively, in Fbn1^C1039G/+ mice, when compared to wild-type mice or Fbn1^C1039G/+ mice treated with TGF-β–neutralizing antibody (top panels). Increased TGF-β signaling, as evidenced by increased nuclear accumulation of pSmad2/3 and periostin expression in Fbn1^C1039G/+ mice, when compared to wild-type mice or mice treated with TGF-β–neutralizing antibody (bottom panels). Morphometric analyses of tibialis anterior muscle 18 d after cardiotoxin injection shows reduced myofiber CSA (in μm²) in Fbn1^C1039G/+ mice, when compared to wild-type mice or Fbn1^C1039G/+ mice treated with TGF-β–neutralizing antibody (graph). Scale bars, 40 μm.