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HSPB3 protein is expressed in motoneurons and induces their survival after lesion-induced degeneration.

Abstract：

:The human small heat shock proteins (HSPBs) form a family of molecular chaperones comprising ten members (HSPB1-HSPB10), whose functions span from protein quality control to cytoskeletal dynamics and cell death control. Mutations in HSPBs can lead to human disease and particularly point mutations in HSPB1 and HSPB8 are known to lead to peripheral neuropathies. Recently, a missense mutation (R7S) in yet another member of this family, HSPB3, was found to cause an axonal motor neuropathy (distal hereditary motor neuropathy type 2C, dHMN2C). Until now, HSPB3 protein localization and function in motoneurons (MNs) have not yet been characterized. Therefore, we studied the endogenous HSPB3 protein distribution in the spinal cords of chicken and mouse embryos and in the postnatal nervous system (central and peripheral) of chicken, mouse and human. We further investigated the impact of wild-type and mutated HSPB3 on MN cell death via overexpressing these genes in ovo in an avian model of MN degeneration, the limb-bud removal. Altogether, our findings represent a first step for a better understanding of the cellular and molecular mechanisms leading to dHMN2C.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

La Padula V,Staszewski O,Nestel S,Busch H,Boerries M,Roussa E,Prinz M,Krieglstein K

doi

10.1016/j.expneurol.2016.08.014

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

40-49

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(16)30253-9

journal_volume

286

pub_type

杂志文章

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