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Identification of a lectin causing the degeneration of neuronal processes using engineered embryonic stem cells
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Identification of a lectin causing the degeneration of neuronal processes using engineered embryonic stem cells
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Identification of a lectin causing the degeneration of neuronal processes using engineered embryonic stem cells
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Journal Article
Identification of a lectin causing the degeneration of neuronal processes using engineered embryonic stem cells
2007
Overview
Unlike the mechanisms involved in the death of neuronal cell bodies, those causing the elimination of processes are not well understood owing to the lack of suitable experimental systems. As the neurotrophin receptor p75
NTR
is known to restrict the growth of neuronal processes, we engineered mouse embryonic stem (ES) cells to express an
Ngfr
(p75
NTR
) cDNA under the control of the
Mapt
locus (the gene encoding tau), which begins to be active when ES cell–derived progenitors start elongating processes. This caused a progressive, synchronous degeneration of all processes, and a prospective proteomic analysis showed increased levels of the sugar-binding protein galectin-1 in the p75
NTR
-engineered cells. Function-blocking galectin-1 antibodies prevented the degeneration of processes, and recombinant galectin-1 caused the processes of wild-type neurons to degenerate first, followed by the cell bodies.
In vivo
, the application of a glutamate receptor agonist, a maneuver known to upregulate p75
NTR
, led to an increase in the amount of galectin-1 and to the degeneration of neurons and their processes in a galectin-1–dependent fashion. Section of the sciatic nerve also rapidly upregulated levels of p75
NTR
and galectin-1 in terminal Schwann cells, and the elimination of nerve endings was delayed at the neuromuscular junction of mice lacking
Lgals1
(the gene encoding galectin-1). These results indicate that galectin-1 actively participates in the elimination of neuronal processes after lesion, and that engineered ES cells are a useful tool for studying relevant aspects of neuronal degeneration that have been hitherto difficult to analyze.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Antibodies - therapeutic use
/ Biomedical and Life Sciences
/ Dose-Response Relationship, Drug
/ Gene Expression Regulation - physiology
/ Identification and classification
/ Lectins
/ Mice
/ Nerve Degeneration - chemically induced
/ Nerve Degeneration - therapy
/ Neuroprotective Agents - pharmacology
/ Protein Engineering - methods
/ Proteins
/ Rats
/ Receptor, Nerve Growth Factor - biosynthesis
/ Receptor, Nerve Growth Factor - therapeutic use
