Erratum | Open | Published:
Erratum to: Thrombospondin 1 is a key mediator of transforming growth factor b-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism
Fibrogenesis & Tissue Repairvolume 8, Article number: 4 (2015)
The original article was published in Fibrogenesis & Tissue Repair 2011 4:9
After publication of this work , the authors became aware of some errors in the figures with respect to the loading controls for the western blots in Figure Two panel A (Figure 1 here), Figure Five panel B (Figure 2 here) and Figure Six panel A (Figure 3 here). These errors were due to genuine mistakes in generating the figures from templates and incorrect cropping of the western blot X-ray film images. These errors had no impact on the scientific conclusions of the article. The experiments reported in these figures have been repeated and new images produced.
Figure Two panel A (Figure 1 here) - Experiment assessing the influence of blocking thrombospopndin- 1 on normal and scleroderma fibroblasts in 3-dimensional collagen gels was performed and western blot for loading control GAPDH as well as total ERK and phospho-ERK were completed.
Figure Five panel B (Figure 2 here) - Role of PDGF, IFNb and TFGb and the influence of the kinase inhibitor Gleevac on MAPK activation by normal fibroblasts was carried out and the levels of total ERK and phospho-ERK assessed.
Figure Six panel B (Figure 3 here) - The effect of the ERK inhibitor (U0126) and IFNb on the expression of thrombospondin-1 compared to the loading control (GAPDH) was re-examined in normal and scleroderma fibroblasts.
Yunliang C, Andrew L, Abraham DJ, Laura K, Xu S-w, Denton CP, et al. Thrombospondin 1 is a key mediator of transforming growth factor b-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism. Fibrogenesis and Tissue Repair. 2011;4:9.
The authors declare that they have no competing interests.
The online version of the original article can be found under doi:10.1186/1755-1536-4-9.