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Titolo:
Increased neuronal and glial expression of protein kinase C isoforms in neocortex of transgenic Tg2576 mice with amyloid pathology
Autore:
Rossner, S; Mehlhorn, G; Schliebs, R; Bigl, V;
Indirizzi:
Paul Flechsig Inst Brain Res, Dept Neurochem, D-04109 Leipzig, Germany Paul Flechsig Inst Brain Res Leipzig Germany D-04109 09 Leipzig, Germany
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 2, volume: 13, anno: 2001,
pagine: 269 - 278
SICI:
0953-816X(200101)13:2<269:INAGEO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRECURSOR PROTEIN; ALZHEIMERS-DISEASE; BETA-SECRETASE; IN-VIVO; OXIDATIVE STRESS; PKC ISOFORMS; PC12 CELLS; PEPTIDE; ALPHA; BRAIN;
Keywords:
Alzheimer's disease; amyloid plaques; amyloid precursor protein processing; animal model; astrocytes; gliosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Rossner, S Paul Flechsig Inst Brain Res, Dept Neurochem, Jahnallee 59, D-04109 Leipzig, Germany Paul Flechsig Inst Brain Res Jahnallee 59 Leipzig Germany D-04109
Citazione:
S. Rossner et al., "Increased neuronal and glial expression of protein kinase C isoforms in neocortex of transgenic Tg2576 mice with amyloid pathology", EUR J NEURO, 13(2), 2001, pp. 269-278

Abstract

We investigated the influence of five- to sevenfold neuronal overexpression of the Swedish mutation of human APP695 (APPsw) in the transgenic mouse strain Tg2576 on neocortical protein kinase C (PKC) expression and subcellular distribution. Using specific antibodies to PKC alpha, PKC beta, PKC gamma, PKC epsilon and PKC zeta isoforms for Western blot analysis, we observedincreased immunoreactivity for PKC alpha and PKC gamma isoforms in crude tissue homogenates from the neocortex of 16-month-old APPsw mice as comparedwith nontransgenic littermates, which was not present in 6 month-old Tg2576 mice. We also observed elevated levels of PKC alpha, PKC beta, PKC gamma and PKC zeta in membrane fractions and reduced concentrations of PKC alpha and PKC gamma in cytosolic fractions of aged Tg2576 mice, indicating that these PKC isoforms are in their activated state. In young, 6-month-old Tg2576 mice, however, the increase in membrane-bound PKC isoforms and concomitant decrease in cytosolic PKC isoforms was much less pronounced, demonstrating the age-dependent nature of alterations in PKC isoforms. Immunocytochemistry of brain sections supported these findings and revealed increased neuronal labelling for PKC alpha, PKC gamma and PKC lambda isoforms in neocortexof 16-month-old APPsw mice compared with nontransgenic littermates, with the increase being strongest for PKC gamma and PKC lambda isoforms. Additionally, PKC gamma and to a lesser extent PKC lambda isoforms were induced in reactive astrocytes in proximity to amyloid plaques. Our data indicate thatneuronal overexpression of APPsw causes a dynamic change in neuronal expression and activation of multiple PKC isoforms known to be regulators of proteolytic amyloid precursor protein (APP) processing (PKC alpha) and of neuronal survival (PKC lambda and PKC zeta). The induction of the PKC gamma andPKC lambda isoforms in reactive astrocytes surrounding amyloid plaques might be required for astrocyte activation and astrocytic cytokine expression in response to amyloid plaque formation.

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Documento generato il 18/01/20 alle ore 08:01:54