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Abstract #23427 Published in IGR 11-2
Muscarinic activation attenuates abnormal processing of β-amyloid precursor protein induced by cobalt chloride-mimetic hypoxia in retinal ganglion cells
Zhu X; Zhou W; Cui Y; Zhu L; Li J; Xia Z; Shao B; Wang H; Chen HBiochemical and Biophysical Research Communications 2009; 384: 110-113
β-Amyloid peptide (Aβ), the major pathological factor in Alzheimer's disease, has recently been reported to be implicated in the development of glaucoma. In this study, we explored the effect of muscarinic activation on abnormal processing of β-amyloid precursor protein (APP) induced by a risk factor hypoxia in retinal ganglion cells. Hypoxia mimetic compound cobalt chloride could increase the generation of Aβ via up-regulating the expression of APP as well as the expression of β-secretase and γ-secretase, whereas muscarinic receptor agonist pilocarpine could significantly attenuate this abnormal pathway, thereby resulting in a decreased amyloidogenic cleavage of APP. This finding may provide an insight into better understanding of pathophysiology for the retinal neurodegenerative disease and searching for its new modifying approach.
H. Chen. Department of Pharmacology, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China. hongzhuan_chen@hotmail.com
Classification:
3.6 Cellular biology (Part of: 3 Laboratory methods)
11.8 Neuroprotection (Part of: 11 Medical treatment)
