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Increased ER-mitochondria tethering promotes axon regeneration

Author(s)
Lee, SoyeonWang, WeiHwang, JinyeonNamgung, UkMin, Kyung-Tai
Issued Date
2019-08
DOI
10.1073/pnas.1818830116
URI
https://scholarworks.unist.ac.kr/handle/201301/27386
Fulltext
https://www.pnas.org/content/116/32/16074
Citation
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.116, no.32, pp.16074 - 16079
Abstract
Translocation of the endoplasmic reticulum (ER) and mitochondria to the site of axon injury has been shown to facilitate axonal regeneration; however, the existence and physiological importance of ER-mitochondria tethering in the injured axons are unknown. Here, we show that a protein linking ER to mitochondria, the glucose regulated protein 75 (Grp75), is locally translated at axon injury site following axotomy, and that overexpression of Grp75 in primary neurons increases ER-mitochondria tethering to promote regrowth of injured axons. We find that increased ER-mitochondria tethering elevates mitochondrial Ca2+ and enhances ATP generation, thereby promoting regrowth of injured axons. Furthermore, intrathecal delivery of lentiviral vector encoding Grp75 to an animal with sciatic nerve crush injury enhances axonal regeneration and functional recovery. Together, our findings suggest that increased ER-mitochondria tethering at axonal injury sites may provide a therapeutic strategy for axon regeneration.
Publisher
NATL ACAD SCIENCES
ISSN
0027-8424
Keyword (Author)
axon regenerationmitochondriaER
Keyword
LIVING CELLSPC12 CELLSAPOPTOSISVISUALIZATIONTRANSPORTPROTECTSENDOPLASMIC-RETICULUMINTRINSIC CONTROLOXIDATIVE STRESSCONTACT SITES

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