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. Author manuscript; available in PMC: 2015 Jul 30.
Published in final edited form as: Gut. 2014 Jul 23;63(11):1693–1694. doi: 10.1136/gutjnl-2014-307712

Figure 1.

Figure 1

Osteopontin (OPN) is an important regulator of the interaction between ductular reaction (DR) cells and hepatic stellate cells (HSC): it may represent a molecular target for therapeutic interference. Following chronic liver injury, OPN produced by DR cells, including hepatic progenitor cell (HPC), stimulates HSC recruitment and activation into myofibroblasts, where it induces transforming growth factor-β signalling and increased collagen deposition; on the parenchymal side, OPN simulates HPC proliferation and migration, while concomitantly downregulating hepatocyte proliferation (green arrow). OPN blockade by specific aptamers or neutralising antibodies halts the crosstalk between DR cells and HSC, thereby hampering myofibroblast activation and reducing matrix production, while turning up hepatocyte proliferation (red arrow).