Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells

October 20, 2009

Activated protein C (APC) is an endogenous plasma protease with anticoagulant activity and direct cytoprotective activities (1). The anticoagulant action of APC is mediated by irreversible proteolytic inactivation of factors Va and VIIIa in plasma with contributions of different cofactors. Independent of its anticoagulant action, the protein C cellular pathway mediates cytoprotective alterations in gene expression (24) and controls activation of several transcription factors that regulate different antiapoptotic and antiinflammatory pathways (2, 46). Most studies have indicated that protease activated receptor–1 (PAR1) is a key receptor mediating APC’s transmembrane signaling in different cell types (1). APC protects neurons (7) and endothelial cells (810) from different types of injury and limits brain damage in rodent models of ischemia (6, 1113) and multiple sclerosis (14). Whether APC can influence a chronic neurodegenerative process like that in amyotrophic lateral sclerosis (ALS) is unknown.

To read the full story, click the following link:

http://www.jci.org/articles/view/38476

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2 Responses to “Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells”

  1. tony said

    Can this help you Rich?

  2. bokeh123 said

    Rich, you tested negative for the SOD1 gene mutation, correct?

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