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Int. J. Mol. Sci. 2017, 18(7), 1442; doi:10.3390/ijms18071442

Early Hippocampal i-LTP and LOX-1 Overexpression Induced by Anoxia: A Potential Role in Neurodegeneration in NPC Mouse Model

1
Department of Medical System, University of Rome Tor Vergata, Rome 00133, Italy
2
Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome 00133, Italy
3
CNMR, Istituto Superiore di Sanità Roma, Rome 00161, Italy
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 13 June 2017 / Revised: 26 June 2017 / Accepted: 29 June 2017 / Published: 5 July 2017
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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Abstract

Niemann-Pick type C disease (NPCD) is an autosomal recessive storage disorder, characterized by abnormal sequestration of unesterified cholesterol within the late endo-lysosomal compartment of cells. In the central nervous system, hypoxic insults could result in low-density lipoprotein (LDL) oxidation and Lectin-like oxidized LDL receptor-1 (LOX-1) induction, leading to a pathological hippocampal response, namely, ischemic long-term potentiation (i-LTP). These events may correlate with the progressive neural loss observed in NPCD. To test these hypotheses, hippocampal slices from Wild Type (WT) and NPC1−/− mice were prepared, and field potential in the CA1 region was analyzed during transient oxygen/glucose deprivation (OGD). Moreover, LOX-1 expression was evaluated by RT-qPCR, immunocytochemical, and Western blot analyses before and after an anoxic episode. Our results demonstrate the development of a precocious i-LTP in NPC1−/− mice during OGD application. We also observed a higher expression of LOX-1 transcript and protein in NPC1−/− mice with respect to WT mice; after anoxic damage to LOX-1 expression, a further increase in both NPC1−/− and WT mice was observed, although the protein expression seems to be delayed, suggesting a different kinetic of induction. These data clearly suggest an elevated susceptibility to neurodegeneration in NPC1−/− mice due to oxidative stress. The observed up-regulation of LOX-1 in the hippocampus of NPC1−/− mice may also open a new scenario in which new biomarkers can be identified. View Full-Text
Keywords: NPCD; neurodegeneration; i-LTP; LOX-1 NPCD; neurodegeneration; i-LTP; LOX-1
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Lo Castro, A.; Murdocca, M.; Pucci, S.; Zaratti, A.; Greggi, C.; Sangiuolo, F.; Tancredi, V.; Frank, C.; D’Arcangelo, G. Early Hippocampal i-LTP and LOX-1 Overexpression Induced by Anoxia: A Potential Role in Neurodegeneration in NPC Mouse Model. Int. J. Mol. Sci. 2017, 18, 1442.

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