Increased expression of connexin 43 in a mouse model of spinal motoneuronal loss.

Abstract:

:Amyotrophic lateral sclerosis (ALS) is one of the most common motoneuronal disease, characterized by motoneuronal loss and progressive paralysis. Despite research efforts, ALS remains a fatal disease, with a survival of 2-5 years after disease onset. Numerous gene mutations have been correlated with both sporadic (sALS) and familiar forms of the disease, but the pathophysiological mechanisms of ALS onset and progression are still largely uncertain. However, a common profile is emerging in ALS pathological features, including misfolded protein accumulation and a cross-talk between neuroinflammatory and degenerative processes. In particular, astrocytes and microglial cells have been proposed as detrimental influencers of perineuronal microenvironment, and this role may be exerted via gap junctions (GJs)- and hemichannels (HCs)-mediated communications. Herein we investigated the role of the main astroglial GJs-forming connexin, Cx43, in human ALS and the effects of focal spinal cord motoneuronal depletion onto the resident glial cells and Cx43 levels. Our data support the hypothesis that motoneuronal depletion may affect glial activity, which in turn results in reactive Cx43 expression, further promoting neuronal suffering and degeneration.

journal_name

Aging (Albany NY)

journal_title

Aging

authors

Spitale FM,Vicario N,Rosa MD,Tibullo D,Vecchio M,Gulino R,Parenti R

doi

10.18632/aging.103561

subject

Has Abstract

pub_date

2020-06-24 00:00:00

pages

12598-12608

issue

13

issn

1945-4589

pii

103561

journal_volume

12

pub_type

杂志文章

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