Recent evidence indicates that A beta oligomers are recruited at the synapse, oppose expression of long-term potentiation (LTP), perturb intracellular calcium balance, disrupt dendritic spines, and induce memory deficits. However, the molecular mechanisms behind these outcomes are only partially understood; achieving such insight is necessary for the comprehension of A beta-mediated EVP4593 neuronal dysfunction. We have investigated the role of the phosphatase calcineurin (CaN) in these pathological processes of AD. CaN is especially abundant in the CNS, where
it is involved in synaptic activity, LTP, and memory function. Here, we describe how oligomeric A beta treatment causes memory deficits and depresses LIP expression in a CaN-dependent fashion. Mice given
a single intracerebroventricular injection of A beta oligomers exhibited increased CaN activity and decreased pCREB, a transcription factor involved in proper LBH589 concentration synaptic function, accompanied by decreased memory in a fear conditioning task. These effects were reversed by treatment with the CaN inhibitor FK506. We further found that expression of hippocampal LIP in acutely cultured rodent brain slices was opposed by A beta oligomers and that this effect was also reversed by FK506. Collectively, these results indicate that CaN activation may play a central
role in mediating synaptic and memory disruption induced by acute oligonneric A beta treatment in mice. (C) 2010 Wiley-Liss, Inc.”
“Background. To investigate the expression of periostin in breast cancer and its clinical relevance.\n\nMethods. Periostin mRNA expression in LY333531 breast tissues was measured by RT-PCR. Periostin protein in breast tissues was evaluated by Western blot. Immunohistochemistry method (Envision method) was carried out to detect the expression of periostin in breast cancer tissues of different clinical stages and metastasized lymph nodes, as well as benign breast disease.\n\nResults. The expression of periostin in cancer tissue was increased at both mRNA level (P < 0.05) and protein level (P < 0.05) compared with benign and normal breast tissues. The periostin protein expression level increased with breast cancer clinical stages as shown by IHC.\n\nConclusion. Periostin was overexpressed in breast cancer tissues as opposed to normal breast, which implies its role in the pathogenesis and development of this disorder. (C) 2010 Elsevier Inc. All rights reserved.