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Atg5 deficit exaggerates the lysosome formation and cathepsin B activation in mice brain after lipid nanoparticles injection.
- Source :
-
Nanomedicine : nanotechnology, biology, and medicine [Nanomedicine] 2014 Nov; Vol. 10 (8), pp. 1843-52. Date of Electronic Publication: 2014 Apr 22. - Publication Year :
- 2014
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Abstract
- The present study was designed to investigate the role of autophagy-lysosome signaling in the brain after application of nanoparticles. Here, lipid nanoparticles (LNs) induced elevations of Atg5, P62, LC3 and cathepsin B in mice brain. The transmission electron microscopy revealed a dramatic elevation of lysosome vacuoles colocalized with LNs cluster inside the neurons in mice brain. Immunoblot data revealed abnormal expression of cathepsin B in brain cortex following LNs injection, whereas its expression was further elevated in Atg5(+/-) mice. The importance of Atg5 in the LNs-induced autophagy-lysosome cascade was further supported by our finding that neurovascular response was exaggerated in Atg5(+/-) mice. In addition, the siRNA knockdown of Atg5 significantly blunted the increasing of LC3 and P62 in LNs-treated Neuro-2a cells. Taken together, we propose that LNs induce autophagy-lysosome signaling and neurovascular response at least partially via an Atg5-dependent pathway.<br />From the Clinical Editor: These authors investigated autophagy-lysosome signaling in the mouse brain after application of lipid nanoparticles and report that these nanoparticles induce autophagy-lysosome signaling and neurovascular response at least partially via an Atg5-dependent pathway.<br /> (Copyright © 2014 Elsevier Inc. All rights reserved.)
Details
- Language :
- English
- ISSN :
- 1549-9642
- Volume :
- 10
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Nanomedicine : nanotechnology, biology, and medicine
- Publication Type :
- Academic Journal
- Accession number :
- 24768629
- Full Text :
- https://doi.org/10.1016/j.nano.2014.03.019