| First Author | Igbavboa U | Year | 2006 |
| Journal | Neuroscience | Volume | 142 |
| Issue | 3 | Pages | 655-60 |
| PubMed ID | 16904834 | Mgi Jnum | J:113143 |
| Mgi Id | MGI:3664671 | Doi | 10.1016/j.neuroscience.2006.06.056 |
| Citation | Igbavboa U, et al. (2006) Amyloid beta-protein(1-42) increases cAMP and apolipoprotein E levels which are inhibited by beta(1) and beta(2)-adrenergic receptor antagonists in mouse primary astrocytes. Neuroscience 142(3):655-60 |
| abstractText | Amyloid 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. |
