Literature DB >> 18176559

NGF-promoted axon growth and target innervation requires GITRL-GITR signaling.

Gerard W O'Keeffe1, Humberto Gutierrez, Pier Paolo Pandolfi, Carlo Riccardi, Alun M Davies.   

Abstract

Nerve growth factor (NGF) has an important role in regulating sympathetic neuron survival and target field innervation during development. Here we show that glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR), a member of the TNF superfamily, and its ligand (GITRL) are co-expressed in mouse sympathetic neurons when their axons are innervating their targets under the influence of target-derived NGF. In culture, GITRL enhanced NGF-promoted neurite growth from neonatal sympathetic neurons, and preventing GITR-GITRL interaction in these neurons or knocking down GITR inhibited NGF-promoted neurite growth without affecting neuronal survival. Tnfrsf18(-/-) (Gitr) neonates have reduced sympathetic innervation density in vivo compared with Gitr(+/+) littermates. GITR activation is required for the phosphorylation of extracellular signal-regulated kinases 1 and 2 by NGF that is necessary for neurite growth. Our results reveal a previously unknown signaling loop in developing sympathetic neurons that is crucial for NGF-dependent axon growth and target innervation.

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Year:  2008        PMID： 18176559      PMCID： PMC3531920          DOI： 10.1038/nn2034

Source DB:  PubMed          Journal:  Nat Neurosci        ISSN： 1097-6256            Impact factor:   24.884


  31 in total

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  38 in total

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