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Somatostatin stimulates the migration of hepatic oval cells in the injured rat liver
Author(s) -
Jung Youngmi,
Oh SehHoon,
Witek Rafal P.,
Petersen Bryon E.
Publication year - 2012
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2011.02642.x
Subject(s) - somatostatin , somatostatin receptor , somatostatin receptor 2 , medicine , phosphatidylinositol , chemistry , biology , endocrinology , pharmacology , microbiology and biotechnology , kinase
Background Somatostatin 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 ( SSTR 4) respectively. Aims We investigated the in vivo effect of somatostatin/ SSTR 4 on HOC migration in the injured liver model of rats and the type of signalling molecules associated with the chemotactic function. Methods Migration assay, HOC transplantation and phosphatidylinositol‐3‐kinase ( PI3K ) signalling were assessed with or without somatostatin and an analogue of somatostatin ( TT 232) that specifically binds to SSTR 4. Results TT 232 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 TT 232‐treated animals, as compared with control animals. Activation of PI3K was observed in HOC exposed to somatostatin, and this activation was suppressed by either SSTR 4 antibody or TT 232‐pretreatment. In addition, a PI3K inhibitor abrogated the motility of HOC . Conclusion Together, these data suggest that somatostatin stimulates the migration of HOC within injured liver through SSTR 4, and this action appears to be mediated by the PI3K pathway.