Elevating Growth Factor Responsiveness and Axon Regeneration by Modulating Presynaptic Inputs.

Szczegóły
Abstrakt

Tytuł:: Elevating Growth Factor Responsiveness and Axon Regeneration by Modulating Presynaptic Inputs.
Autorzy:: Zhang Y; F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Williams PR; F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA; Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: .
Jacobi A; F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Wang C; F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Goel A; Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA.
Hirano AA; Department of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; United States Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Brecha NC; Department of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; United States Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Kerschensteiner D; Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA.
He Z; F.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Źródło:: Neuron [Neuron] 2019 Jul 03; Vol. 103 (1), pp. 39-51.e5. Date of Electronic Publication: 2019 May 20.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
Język:: English
Imprint Name(s):: Original Publication: [Cambridge, Mass. : Cell Press, c1988-
MeSH Terms:: Axons/*physiology
Nerve Growth Factor/*physiology
Nerve Regeneration/*physiology
Receptors, Presynaptic/*physiology
Amacrine Cells/physiology ; Animals ; Cilia/metabolism ; Cilia/ultrastructure ; Insulin-Like Growth Factor I/pharmacology ; Mice ; Mice, Inbred C57BL ; Nerve Crush ; Optic Nerve Injuries/pathology ; RNA-Binding Proteins/genetics ; Receptor, IGF Type 1/metabolism ; Retina/metabolism ; Retinal Ganglion Cells/drug effects
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Grant Information:: R01 EY029869 United States EY NEI NIH HHS; R01 EY015573 United States EY NEI NIH HHS; P30 HD018655 United States HD NICHD NIH HHS; P30 EY012196 United States EY NEI NIH HHS; R01 EY027411 United States EY NEI NIH HHS; R01 EY026978 United States EY NEI NIH HHS; IK6 BX005230 United States BX BLRD VA; I01 BX000764 United States BX BLRD VA; R01 EY023341 United States EY NEI NIH HHS
Substance Nomenclature:: 0 (Lin-28 protein, mouse)
0 (RNA-Binding Proteins)
0 (Receptors, Presynaptic)
67763-96-6 (Insulin-Like Growth Factor I)
9061-61-4 (Nerve Growth Factor)
EC 2.7.10.1 (Receptor, IGF Type 1)
Entry Date(s):: Date Created: 20190525 Date Completed: 20191022 Latest Revision: 20210604
Update Code:: 20240104
PubMed Central ID:: PMC7350660
DOI:: 10.1016/j.neuron.2019.04.033
PMID:: 31122676
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Despite robust effects on immature neurons, growth factors minimally promote axon regeneration in the adult central nervous system (CNS). Attempting to improve growth-factor responsiveness in mature neurons by dedifferentiation, we overexpressed Lin28 in the retina. Lin28-treated retinas responded to insulin-like growth factor-1 (IGF1) by initiating retinal ganglion cell (RGC) axon regeneration after axotomy. Surprisingly, this effect was cell non-autonomous. Lin28 expression was required only in amacrine cells, inhibitory neurons that innervate RGCs. Ultimately, we found that optic-nerve crush pathologically upregulated activity in amacrine cells, which reduced RGC electrical activity and suppressed growth-factor signaling. Silencing amacrine cells or pharmacologically blocking inhibitory neurotransmission also induced IGF1 competence. Remarkably, RGCs regenerating across these manipulations localized IGF1 receptor to their primary cilia, which maintained their signaling competence and regenerative ability. Thus, our results reveal a circuit-based mechanism that regulates CNS axon regeneration and implicate primary cilia as a regenerative signaling hub.
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