Neurotrophins acting through Trk signal-transducing receptors play essential roles in the nervous system, and probably in some non-neuronal tissues. In the present study, we used RT-PCR, Western-blot and immunohistochemistry to investigate the occurrence and cellular localization of TrkB in the mouse liver, from newborns to 6 months. Furthermore, the structure of the liver in mice carrying a mutation in the trkB gene, resulting in a non-functional protein, was studied. The analysis of the DNA sequence showed that hepatic trkB gene is identical to the cerebral one, and TrkB mRNA and TrkB full-length protein (145 kDa) were detected at all the ages sampled. Immunohistochemistry revealed age-dependent changes in the pattern of TrkB expression. From 0 to 15 days, the TrkB was detected in morphologically and immunohistochemically identified monocyte-macrophage-dendric cells scattered throughout the organ, while in animals 3- and 6-months-old it was restricted to nerve fibres. Interestingly, there was a parallelism between TrkB expression by monocyte-macrophage-dendric cells and the presence of hepatic erythroblastic islands. In agreement with a possible role of TrkB on hepatic haematopoiesis, the liver of 15 days old TrkB (-/-) mice still contained erythroblastic islands, whereas they were absent in the wild-type littermates. Another striking finding was the absence of nerve profiles in the TrkB (-/-) animals. All together, present results support the role of TrkB in the murine liver in maintaining the innervation of the organ, and more importantly throughout an unknown mechanism in controlling the hepatic haematopoietic function.

Expression of the neurotrophin receptor TrkB in the mouse liver

GERMANA', Antonino;CIRIACO, Emilia;
2006-01-01

Abstract

Neurotrophins acting through Trk signal-transducing receptors play essential roles in the nervous system, and probably in some non-neuronal tissues. In the present study, we used RT-PCR, Western-blot and immunohistochemistry to investigate the occurrence and cellular localization of TrkB in the mouse liver, from newborns to 6 months. Furthermore, the structure of the liver in mice carrying a mutation in the trkB gene, resulting in a non-functional protein, was studied. The analysis of the DNA sequence showed that hepatic trkB gene is identical to the cerebral one, and TrkB mRNA and TrkB full-length protein (145 kDa) were detected at all the ages sampled. Immunohistochemistry revealed age-dependent changes in the pattern of TrkB expression. From 0 to 15 days, the TrkB was detected in morphologically and immunohistochemically identified monocyte-macrophage-dendric cells scattered throughout the organ, while in animals 3- and 6-months-old it was restricted to nerve fibres. Interestingly, there was a parallelism between TrkB expression by monocyte-macrophage-dendric cells and the presence of hepatic erythroblastic islands. In agreement with a possible role of TrkB on hepatic haematopoiesis, the liver of 15 days old TrkB (-/-) mice still contained erythroblastic islands, whereas they were absent in the wild-type littermates. Another striking finding was the absence of nerve profiles in the TrkB (-/-) animals. All together, present results support the role of TrkB in the murine liver in maintaining the innervation of the organ, and more importantly throughout an unknown mechanism in controlling the hepatic haematopoietic function.
2006
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/1676549
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