Abstract
Signaling pathways mediated by the mechanistic target of rapamycin (mTOR) play key roles in aging and age-related diseases. As a downstream protein of mTOR, transcription factor EB (TFEB) controls lysosome biogenesis and cellular trafficking, processes that are essential for the functions of phagocytic cells like the retinal pigment epithelium (RPE). In the current study, we show that a naturally occurring polyphenolic compound, quercetin, promoted TFEB nuclear translocation and enhanced its transcriptional activity in cultured RPE cells. Activated TFEB facilitated degradation of phagocytosed photoreceptor outer segments. Quercetin is a direct inhibitor of mTOR but did not influence the activity of Akt at the tested concentration range. Our data suggest that the dietary compound quercetin can have beneficial roles in neuronal tissues by improving the functions of the TFEB-lysosome axis and enhancing the capacities of cellular degradation and self-renewal.
Original language | English (US) |
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Number of pages | 1 |
Journal | Oxidative Medicine and Cellular Longevity |
Volume | 2018 |
DOIs | |
State | Published - Jan 1 2018 |
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ASJC Scopus subject areas
- Biochemistry
- Aging
- Cell Biology
Cite this
Enhancing TFEB-Mediated Cellular Degradation Pathways by the mTORC1 Inhibitor Quercetin. / Huang, Yi; Chen, Yan; Shaw, Amanda Marie; Goldfine, Howard; Tian, Junqiang; Cai, Jiyang.
In: Oxidative Medicine and Cellular Longevity, Vol. 2018, 01.01.2018.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Enhancing TFEB-Mediated Cellular Degradation Pathways by the mTORC1 Inhibitor Quercetin
AU - Huang, Yi
AU - Chen, Yan
AU - Shaw, Amanda Marie
AU - Goldfine, Howard
AU - Tian, Junqiang
AU - Cai, Jiyang
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Signaling pathways mediated by the mechanistic target of rapamycin (mTOR) play key roles in aging and age-related diseases. As a downstream protein of mTOR, transcription factor EB (TFEB) controls lysosome biogenesis and cellular trafficking, processes that are essential for the functions of phagocytic cells like the retinal pigment epithelium (RPE). In the current study, we show that a naturally occurring polyphenolic compound, quercetin, promoted TFEB nuclear translocation and enhanced its transcriptional activity in cultured RPE cells. Activated TFEB facilitated degradation of phagocytosed photoreceptor outer segments. Quercetin is a direct inhibitor of mTOR but did not influence the activity of Akt at the tested concentration range. Our data suggest that the dietary compound quercetin can have beneficial roles in neuronal tissues by improving the functions of the TFEB-lysosome axis and enhancing the capacities of cellular degradation and self-renewal.
AB - Signaling pathways mediated by the mechanistic target of rapamycin (mTOR) play key roles in aging and age-related diseases. As a downstream protein of mTOR, transcription factor EB (TFEB) controls lysosome biogenesis and cellular trafficking, processes that are essential for the functions of phagocytic cells like the retinal pigment epithelium (RPE). In the current study, we show that a naturally occurring polyphenolic compound, quercetin, promoted TFEB nuclear translocation and enhanced its transcriptional activity in cultured RPE cells. Activated TFEB facilitated degradation of phagocytosed photoreceptor outer segments. Quercetin is a direct inhibitor of mTOR but did not influence the activity of Akt at the tested concentration range. Our data suggest that the dietary compound quercetin can have beneficial roles in neuronal tissues by improving the functions of the TFEB-lysosome axis and enhancing the capacities of cellular degradation and self-renewal.
UR - http://www.scopus.com/inward/record.url?scp=85060935311&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85060935311&partnerID=8YFLogxK
U2 - 10.1155/2018/5073420
DO - 10.1155/2018/5073420
M3 - Article
C2 - 30510622
AN - SCOPUS:85060935311
VL - 2018
JO - Oxidative Medicine and Cellular Longevity
JF - Oxidative Medicine and Cellular Longevity
SN - 1942-0900
ER -