hdac6 regulates epidermal growth factor receptor (egfr) endocytic trafficking and degradation in renal epithelial cellshdac6调节表皮生长因子受体(egfr)在肾上皮细胞内吞作用的走私和退化.pdfVIP
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hdac6 regulates epidermal growth factor receptor (egfr) endocytic trafficking and degradation in renal epithelial cellshdac6调节表皮生长因子受体(egfr)在肾上皮细胞内吞作用的走私和退化
HDAC6 Regulates Epidermal Growth Factor Receptor
(EGFR) Endocytic Trafficking and Degradation in Renal
Epithelial Cells
Wei Liu1,3,4, Lucy X. Fan1,3, Xia Zhou1,3, William E. Sweeney, Jr.1,3, Ellis D. Avner1,2,3, Xiaogang Li1,2,3*
1 Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America, 2 Department of Physiology, Medical College of Wisconsin,
Milwaukee, Wisconsin, United States of America, 3 Children’s Research Institute, Children’s Hospital of Wisconsin, Milwaukee, Wisconsin, United States of America,
4 Department of Nephrology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China
Abstract
We present for the first time that histone deacetylase 6 (HDAC6) regulates EGFR degradation and trafficking along
microtubules in Pkd1 mutant renal epithelial cells. HDAC6, the microtubule-associated a-tubulin deacetylase, demonstrates
increased expression and activity in Pkd1 mutant mouse embryonic kidney cells. Targeting HDAC6 with a general HDAC
inhibitor, trichostatin (TSA), or a specific HDAC6 inhibitor, tubacin, increased the acetylation of a-tubulin and downregulated
the expression of EGFR in Pkd1 mutant renal epithelial cells. HDAC6 was co-localized with EGF induced endocytic EGFR and
endosomes, respectively. Inhibition of the activity of HDAC6 accelerated the trafficking of EGFR from early endosomes to
late endosomes along the microtubules. Without EGF stimulation EGFR was randomly distributed while after stimulation
with EGF for 30 min, EGFR was accumulated around a-tubulin labeled microtubule bundles. These data suggested that the
Pkd1 mutation induced upregulation of HDAC6 might act to slow the trafficking of EGFR from early endosomes to late
endosomes along the microtubules for degradation through deacetylating a-tubulin. In addition, inhibition of H
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