Amyloid beta-protein1-42 increases cAMP and apolipoprotein E levels which are inhibited by β1 and β2-adrenergic receptor antagonists in mouse primary astrocytes
2006; Elsevier BV; Volume: 142; Issue: 3 Linguagem: Inglês
10.1016/j.neuroscience.2006.06.056
ISSN1873-7544
AutoresUrule Igbavboa, Leslie N. Johnson‐Anuna, Ximena Serenella Rossello, Tammy A. Butterick, Grace Y. Sun, W. G. Wood,
Tópico(s)Neuroscience and Neuropharmacology Research
ResumoAmyloid beta-protein (Abeta) increases apolipoprotein E (apoE) levels in astrocytes which could alter lipid trafficking. The mechanism for the Abeta-induced increase in apoE levels is not well understood. It is well established that stimulation of beta-adrenergic receptors (betaARs) increases cAMP levels. Elevation of cAMP levels increases apoE abundance. The current study determined if Abeta(1-42) stimulation of cAMP and apoE levels could be inhibited by betaAR antagonists in astrocytes. We demonstrate that Abeta(1-42) but not the reverse protein Abeta(42-1) or Abeta(1-40) stimulated cAMP formation and this stimulation was inhibited by selective betaAR antagonists in mouse primary cortical astrocytes. Abeta(1-42) significantly increased apoE levels which were significantly inhibited by the betaAR selective antagonists with the greatest inhibition observed with the beta(2) antagonist. Separate lines of evidence have suggested that agonist-induced stimulation of betaARs and increases in apoE abundance may serve a neuroprotective role in astrocytes. Our results indicate a potential interaction between betaARs and apoE which may contribute to reducing Abeta(1-42) neurotoxicity.
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