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Inhibition of microtubule dynamics impedes repair of kidney ischemia/reperfusion injury and increases fibrosis

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Author(s)
Sang Jun HanJi-Hyeon KimJee In KimKwon Moo Park
Keimyung Author(s)
Kim, Jee In
Department
Dept. of Molecular Medicine (분자의학)
Journal Title
Scientific Reports.
Issued Date
2016
Volume
6
Issue
27775
Abstract
The microtubule cytoskeleton is composed of α-tubulin and β-tubulin heterodimers, and it serves
to regulate the shape, motility, and division of a cell. Post-translational modifications including
acetylation are closely associated with the functional aspects of the microtubule, involving in a number
of pathological diseases. However, the role of microtubule acetylation in acute kidney injury (AKI)
and progression of AKI to chronic kidney disease have yet to be understood. In this study, ischemia/
reperfusion (I/R), a major cause of AKI, resulted in deacetylation of the microtubules with a decrease
in α-tubulin acetyltransferase 1 (α-TAT1). Paclitaxel (taxol), an agent that stabilizes microtubules
by tubulin acetylation, treatment during the recovery phase following I/R injury inhibited tubular
cell proliferation, impaired renal functional recovery, and worsened fibrosis. Taxol induced α-tubulin
acetylation and post-I/R cell cycle arrest. Taxol aggregated the microtubule in the cytoplasm, resulting
in suppression of microtubule dynamics. Our studies have demonstrated for the first time that I/R
induced deacetylation of the microtubules, and that inhibition of microtubule dynamics retarded repair
of injured tubular epithelial cells leading to an acceleration of fibrosis. This suggests that microtubule
dynamics plays an important role in the processes of repair and fibrosis after AKI.
Keimyung Author(s)(Kor)
김지인
Publisher
School of Medicine
Citation
Sang Jun Han et al. (2016). Inhibition of microtubule dynamics impedes repair of kidney ischemia/reperfusion injury and increases fibrosis. Scientific Reports., 6(27775), 1–13. doi: 10.1038/srep27775
Type
Article
ISSN
2045-2322
DOI
10.1038/srep27775
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/33220
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Molecular Medicine (분자의학)
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