Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 15 P211

Division of Neuroscience and Mental Health, Imperial College Faculty of Medicine, Du Cane Road, London, UK.


The main pathological finding in Parkinson’s disease (PD) is the loss of dopaminergic cells in the substantia nigra (SNc). Current dopamine-replacement therapies alleviate symptoms but do not prevent disease progression. The pathophysiology of PD is unknown, but oxidative stress and neuroinflammation have been implicated. A better understanding of the cause of dopaminergic cell death may lead to the discovery of new therapies that can slow disease progression.

Annexin A1 (ANXA1), a 37 kDa protein, is implicated in PD by its presence in glial scars of Parkinsonian SNc. It has been shown to reduce inflammation and induce apoptosis in a number of inflammatory cell lines. Thus ANXA1 might play a neuroprotective role in PD by acting as an anti-inflammatory mediator in the SNc.

This study used PC12 cells differentiated with nerve growth factor (NGF) to model dopaminergic cells in order to investigate the direct effect of ANXA1 and a known neurotoxin, 6-hydroxydopamine, on their apoptosis. Using FACS-analysis the results established that PC12 cells do not express ANXA1. Hoechst-H33342 staining and the APOPercentage-assay showed for the first time that exogenous ANXA1 induced apoptosis of PC12 cells pre-treated with NGF for 24 h and 7 days. This study also showed that 6-hydroxydopamine induced apoptosis of PC12 cells, but contrastingly, 24 h pre-treatment with NGF protected against its toxicity. The data indicate that ANXA1 is acting as a cell death signal. As this appears to be a mechanism whereby ANXA1 promotes phagocytosis, at least in the periphery (Solito E et al., 2003, FASEB J 17 1544–1546), the results support the view that in vivo ANXA1 could promote phagocytotic clearance of damaged dopaminergic cells, thereby limiting the resultant neuroinflammatory-response and slowing PD progression.

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