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Letter
Role of BMP-9 in human liver disease
  1. Miya John,
  2. Kyung-Jin Kim,
  3. Sarah Da Won Bae,
  4. Liang Qiao,
  5. Jacob George
  1. Storr Liver Centre, The Westmead Institute for Medical Research, University of Sydney and Westmead Hospital, Westmead, New South Wales, Australia
  1. Correspondence to Professor Liang Qiao, Storr Liver Centre, The Westmead Institute for Medical Research, University of Sydney and Westmead Hospital, Westmead NSW 2145, Australia; liang.qiao{at}sydney.edu.au and Professor Jacob George, Storr Liver Centre, The Westmead Institute for Medical Research, University of Sydney and Westmead Hospital Westmead New South Wales Australia ; jacob.george{at}sydney.edu.au

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We read with interest the article by Breitkopf-Heinlein et al,1 investigating the role of bone morphogenetic protein (BMP)-9 in liver regeneration and fibrosis. In mice, the authors demonstrate that BMP-9, a member of the transforming growth factor-β family, is primarily produced by hepatic stellate cells (HSCs) and is a profibrogenic factor. Inhibition or knockout of BMP-9 reduced liver fibrosis, while the recombinant protein increased the proliferation and migration of human HSCs. However, as shown in figure 1H and I of that study, rhBMP-9 did not upregulate fibrosis markers (eg, collagen I, fibronectin, platelet-derived growth factor B and α smooth muscle actin). While BMP-9 expression increased during the activation of primary human HSCs, the authors were unable to demonstrate a correlation between human hepatic BMP-9 expression and liver fibrosis stage from a publicly available microarray dataset.

Figure 1

mRNA expression of BMP-9 pathway genes in human liver disease from microarray data. Boxplots showing BMP-9, BMP-10, Alk1 and ACVR2B mRNA in liver from normal and cirrhosis subjects (A), obese subjects with healthy liver and patients with NASH (B), and patients with mild …

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