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Signaling by growth/differentiation factor 5 through the bone morphogenetic protein receptor type IB protects neurons against kainic acid-induced neurodegeneration.

Abstract：

:Growth/differentiation factor-5 (GDF-5), a member of the transforming growth factor-beta (TGF-β) superfamily, has been shown to protect rat dopaminergic neurons against insult both in embryonic neuronal culture and in Parkinson's disease models. However, whether GDF-5 exerts neuroprotective effects in hippocampal neurons is unclear. Here, we show that both mRNA levels and protein levels of GDF-5 are decreased in the mouse hippocampus upon kainic acid (KA) treatment. KA induced dramatic neuronal loss specifically in the cornu ammonis 1 (CA1) and CA3 areas of the mouse hippocampus, while intracerebral infusion of GDF-5 prevented this neuronal loss. The neuroprotective effects of GDF-5 were recapitulated by constitutively active bone morphogenetic protein type IB receptor (BMPRIB-CA) and could be blocked by BMPRI kinase inhibitor LDN-193189. Furthermore, the neuroprotective effects of GDF-5 were mediated through the prevention of apoptosis, which was indicated by terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) staining and reduced cleaved caspase 3 expression level. Thus, we conclude that GDF-5 protects hippocampal neurons against KA-induced neurodegeneration by signaling through BMPRIB, suggesting a therapeutic potential for GDF-5 in neurodegenerative diseases.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Zhao Y,Zhang M,Liu H,Wang J

doi

10.1016/j.neulet.2017.04.055

subject

Has Abstract

pub_date

2017-06-09 00:00:00

pages

36-42

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(17)30367-1

journal_volume

651

pub_type

杂志文章

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