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Altered calmodulin degradation and signaling in non-neuronal cells from Alzheimer’s disease patients

AuthorsEsteras, Noemí ; Muñoz, Úrsula ; Alquézar, Carolina ; Bartolomé Robledo, Fernando ; Bermejo-Pareja, Félix; Martín-Requero, Ángeles
KeywordsAlzheimer’s disease
homologous domains
Stroke-Alzheimer’s Disease
protein degradation
antioxidants GSH
Issue DateMar-2012
PublisherBentham Science Publishers
CitationCurrent Alzheimer Research 9 (3) : 267-277 (2012)
AbstractPrevious work indicated that changes in Ca2+/calmodulin (CaM) signaling pathway are involved in the control of proliferation and survival of immortalized lymphocytes from Alzheimer’s disease (AD) patients. We examined the regulation of cellular CaM levels in AD lymphoblasts. An elevated CaM content in AD cells was found when compared with control cells from age-matched individuals. We did not find significant differences in the expression of the three genes that encode CaM: CALM1, 2, 3, by real time RT-PCR. However, we observed that the half-life of CaM was higher in lymphoblasts from AD than in control cells, suggesting that degradation of CaM is impaired in AD lymphoblasts. The rate of CaM degradation was found to be dependent on cellular Ca2+ and ROS levels. CaM degradation occurs mainly via the ubiquitin-proteasome system. Increased levels of CaM were associated with overactivation of PI3K/Akt and CaMKII. Our results suggest that increased levels of CaM synergize with serum to overactivate PI3K/Akt in AD cells by direct binding of CaM to the regulatory α-subunit (p85) of PI3K. The systemic failure of CaM degradation, and thus of Ca2+/CaM-dependent signaling pathways, may be important in the etiopathogenesis of AD
Description11 páginas -- PAGS nros. 267-277
Publisher version (URL)http://dx.doi.org/10.2174/156720512800107564
Appears in Collections:(CIB) Artículos
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