ArticleLiver international : official journal of the International Association for the Study of the Liver2012
Somatostatin stimulates the migration of hepatic oval cells in the injured rat liver.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Role of liver progenitors in liver regeneration.Hepatobiliary surgery and nutrition · 2015Review
- Two sides of one coin: massive hepatic necrosis and progenitor cell-mediated regeneration in acute liver failure.Frontiers in physiology · 2015Review
- Role of liver progenitors in acute liver injury.Frontiers in physiology · 2013Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundSomatostatin is a pleiotropic peptide, exerting a variety of effects through its receptor subtypes. Recently, somatostatin has been shown to act as a chemoattractant for haematopoietic progenitor cells and hepatic oval cells (HOC) via receptor subtype 2 and subtype 4 (SSTR4) respectively.
aimsWe investigated the in vivo effect of somatostatin/SSTR4 on HOC migration in the injured liver model of rats and the type of signalling molecules associated with the chemotactic function.
methodsMigration assay, HOC transplantation and phosphatidylinositol-3-kinase (PI3K) signalling were assessed with or without somatostatin and an analogue of somatostatin (TT232) that specifically binds to SSTR4.
resultsTT232 was shown to have an antimigratory action on HOC induced by somatostatin in vitro. In HOC transplantation experiments, a lower number of donor-derived cells were detected in TT232-treated animals, as compared with control animals. Activation of PI3K was observed in HOC exposed to somatostatin, and this activation was suppressed by either SSTR4 antibody or TT232-pretreatment. In addition, a PI3K inhibitor abrogated the motility of HOC.
conclusionTogether, these data suggest that somatostatin stimulates the migration of HOC within injured liver through SSTR4, and this action appears to be mediated by the PI3K pathway.
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