Protein kinase C iota protects neural cells against apoptosis induced by amyloid beta-peptide.

Article Details

Citation

Xie J, Guo Q, Zhu H, Wooten MW, Mattson MP

Protein kinase C iota protects neural cells against apoptosis induced by amyloid beta-peptide.

Brain Res Mol Brain Res. 2000 Oct 20;82(1-2):107-13.

PubMed ID
11042363 [ View in PubMed
]
Abstract

Protein kinase C (PKC) isoforms are increasingly recognized as playing important roles in the regulation of neuronal plasticity and survival. Recent findings from studies of non-neuronal cells suggest that atypical isoforms of PKC can modulate apoptosis in various paradigms. Because increasing data support a role for neuronal apoptosis in the pathogenesis of Alzheimer's disease (AD), we tested the hypothesis that PKCiota (PKCiota) can modify vulnerability of neural cells to apoptosis induced by amyloid beta-peptide (ABP), a cytotoxic peptide linked to neuronal degeneration in AD. Overexpression of PKCiota increased the resistance of PC12 cells to apoptosis induced by ABP. Associated with the increased resistance to apoptosis were improved mitochondrial function and reduced activity of caspases. In addition, ABP-induced increases in levels of oxidative stress and intracellular calcium levels were attenuated in cells overexpressing PKCiota. These findings suggest that PKCiota prevents apoptosis induced by ABP by interrupting the cell death process at a very early step, thereby allowing the cells to maintain ion homeostasis and mitochondrial function.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Protein kinase C iota typeP41743Details