Location of prorenin receptors in primate substantia nigra: effects on dopaminergic cell death
Palabras clave : 
Angiotensin
Dopamine
Microglia
Monkey
Neurodegeneration
Parkinson disease
Renin
Fecha incorporación: 
2010
Editorial : 
Lippincott Williams and Wilkins
ISSN: 
1554-6578
Cita: 
Valenzuela R, Barroso-Chinea P, Villar-Cheda B, Joglar B, Muñoz A, Lanciego JL, et al. Location of prorenin receptors in primate substantia nigra: effects on dopaminergic cell death. J Neuropathol Exp Neurol 2010 Nov;69(11):1130-1142.
Resumen
Angiotensin II acts via angiotensin type 1 receptors and is a major inducer of inflammation and oxidative stress. Local renin-angiotensin systems play a major role in the development of age-related disorders in several tissues. These processes are delayed, but not totally abolished, by blockade of angiotensin signaling. A specific receptor for renin and its precursor prorenin has recently been identified. We previously showed that neurotoxin-induced dopaminergic (DA) cell loss is decreased by inhibition of angiotensin receptors, but the location and functional effects of prorenin receptor (PRR) in the brain, including the DA system, are unknown. In the substantia nigra of Macaca fascicularis and in rat primary mesencephalic cultures, double immunofluorescence analysis revealed PRR immunoreactivity in neurons (including DA neurons) and microglia, but not in astrocytes. Administration of the PRR blocker, handle region peptide, led to a significant decrease in 6-hydroxydopamine-induced DA cell death in the cultures,whereas administration of renin with simultaneous blockade of angiotensin receptors led to an increase in 6-hydroxydopamine-induced cell death. These results suggest that active agent angiotensin II-independent PRR intracellular signaling may contribute to exacerbation of DA cell death in vivo. Therefore, potential neuroprotective strategies for DA neurons in Parkinson disease should address both angiotensin and PRR signaling.

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