Cyclooxygenase-1 is involved in the inhibition of hippocampal neurogenesis after lipopolysaccharide-induced neuroinflammation |
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Authors: | Isabella Russo Panomwat Amornphimoltham Roberto Weigert Sergio Barlati Francesca Bosetti |
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Affiliation: | 1.Molecular Neuroscience Unit; Brain Physiology and Metabolism Section; National Institute on Aging; National Institutes of Health; Bethesda, MD USA;2.Division of Biology and Genetics; Department of Biomedical Sciences and Biotechnologies and National Institute of Neuroscience; University of Brescia; Brescia, Italy;3.Intracellular Membrane Trafficking Unit; Oral and Pharyngeal Cancer Branch; National Institute of Dental and Craniofacial Research; National Institutes of Health; Bethesda, MD USA |
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Abstract: | Growing evidence indicates that neuroinflammation can alter adult neurogenesis by mechanisms as yet unclear. We have previously demonstrated that the neuroinflammatory response and neuronal damage after lipopolysaccharide (LPS) injection is reduced in cyclooxygenase-1 deficient (COX-1-/-) mice. In this study, we investigated the role of CoX-1 on hippocampal neurogenesis during LPS-induced neuroinflammation, using COX-1-/- and wild-type (WT) mice. We found that LPS-induced neuroinflammation resulted in the decrease of proliferation, survival and differentiation of hippocampal progenitor cells in WT but not in COX-1-/- mice. Thus, we demonstrate for the first time that COX-1 is involved in the inhibition of BrdU progenitor cells in proliferation and hippocampal neurogenesis after LPS. These results suggest that COX-1 may represent a viable therapeutic target to reduce neuroinflammation and promote neurogenesis in neurodegenerative diseases with a strong inflammatory component.Key words: neurogenesis, cyclooxygenase-1, lipopolysaccharide, inflammation, brain |
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