tailieunhanh - báo cáo hóa học: " Differential regulation of Aβ42-induced neuronal C1q synthesis and microglial activation"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Differential regulation of Aβ42-induced neuronal C1q synthesis and microglial activation | Journal of Neuroinflammation BioMed Central Research Open Access Differential regulation of Ap42-induced neuronal C1q synthesis and microglial activation Rong Fan and Andrea J Tenner Address Department of Molecular Biology and Biochemistry Institute of Brain Aging and Dementia University of California Irvine Irvine CA 92697 USA Email Rong Fan - rfan@ Andrea J Tenner - atenner@ Corresponding author Published 10 January 2005 Received 18 November 2004 Journal of Neuroinflammation 2005 2 1 doi 1742-2094-2-1 Accepted 10 January 2005 This article is available from http content 2 1 1 2005 Fan and Tenner licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Expression of C1q an early component of the classical complement pathway has been shown to be induced in neurons in hippocampal slices following accumulation of exogenous Ap42. Microglial activation was also detected by surface marker expression and cytokine production. To determine whether C1q induction was correlated with intraneuronal Ap and or microglial activation D- - -2-amino-5-phosphonovaleric acid APV an NMDA receptor antagonist and glycine-arginine-glycineaspartic acid-serine-proline peptide RGD an integrin receptor antagonist which blocks and enhances Ap42 uptake respectively were assessed for their effect on neuronal C1q synthesis and microglial activation. APV inhibited and RGD enhanced microglial activation and neuronal C1q expression. However addition of Ap10-20 to slice cultures significantly reduced Ap42 uptake and microglial activation but did not alter the Ap42-induced neuronal C1q expression. Furthermore Ap10-20 alone triggered C1q production in neurons demonstrating that neither neuronal Ap42 accumulation .