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Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling
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| Zeitschriftentitel: | IUBMB Life |
|---|---|
| Personen und Körperschaften: | , , |
| In: | IUBMB Life, 67, 2015, 6, S. 446-452 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Liu, Ning‐Ning Zhao, Ning Cai, Na Liu, Ning‐Ning Zhao, Ning Cai, Na |
|---|---|
| author |
Liu, Ning‐Ning Zhao, Ning Cai, Na |
| spellingShingle |
Liu, Ning‐Ning Zhao, Ning Cai, Na IUBMB Life Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling Cell Biology Clinical Biochemistry Genetics Molecular Biology Biochemistry |
| author_sort |
liu, ning‐ning |
| spelling |
Liu, Ning‐Ning Zhao, Ning Cai, Na 1521-6543 1521-6551 Wiley Cell Biology Clinical Biochemistry Genetics Molecular Biology Biochemistry http://dx.doi.org/10.1002/iub.1382 <jats:title>Abstract</jats:title><jats:p>Rapamycin, a highly specific inhibitor of mammalian target of rapamycin (mTOR), exhibits significant antitumor/antiangiogenic activity in human cancer cells. Its effect on the retinal pigment epithelial (RPE) cells was rarely investigated. This study assessed the proliferation of hypoxia‐induced RPE and the inhibitory effects of rapamycin using 3‐(4,5‐dimethylthazol‐2‐yl)−2,5‐diphenyltetrazolium bromide (MTT) assay and examined the expression of hypoxia‐inducible factor‐1α (HIF‐1α) and vascular endothelial growth factor (VEGF) in RPE cells with or without rapamycin under normoxic and hypoxic conditions using real‐time PCR and Western blot. We found that hypoxia increased the levels of mTOR, HIF‐1α, and VEGF. The suppression of HIF‐1α and VEGF by rapamycin was associated with dephosphorylation of mTOR and the downstream effector ribosomal protein S6 kinase (P70S6K) and 4E‐binding protein‐1 (4E‐BP1) of mTORC1. Rapamycin only inhibited the protein levels and did not change the mRNA expression of HIF‐1α. No cytotoxicity to the RPE cells by rapamycin was caused under either normoxia or hypoxia. Our data suggest that rapamycin suppresses hypoxia‐induced RPE cell proliferation through a mechanism related to the targeting of mTOR/HIF‐1α/VEGF signaling. Rapamycin may potentially provide a safe and effective novel treatment for choroidal vascular disease. © 2015 IUBMB Life, 67(6):446–452, 2015</jats:p> Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the <scp>/</scp>mTOR/HIF‐1α/VEGF<scp>/</scp> signaling IUBMB Life |
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| title |
Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_unstemmed |
Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_full |
Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_fullStr |
Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_full_unstemmed |
Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_short |
Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_sort |
suppression of the proliferation of hypoxia‐induced retinal pigment epithelial cell by rapamycin through the <scp>scp>mtor/hif‐1α/vegf<scp>scp> signaling |
| topic |
Cell Biology Clinical Biochemistry Genetics Molecular Biology Biochemistry |
| url |
http://dx.doi.org/10.1002/iub.1382 |
| publishDate |
2015 |
| physical |
446-452 |
| description |
<jats:title>Abstract</jats:title><jats:p>Rapamycin, a highly specific inhibitor of mammalian target of rapamycin (mTOR), exhibits significant antitumor/antiangiogenic activity in human cancer cells. Its effect on the retinal pigment epithelial (RPE) cells was rarely investigated. This study assessed the proliferation of hypoxia‐induced RPE and the inhibitory effects of rapamycin using 3‐(4,5‐dimethylthazol‐2‐yl)−2,5‐diphenyltetrazolium bromide (MTT) assay and examined the expression of hypoxia‐inducible factor‐1α (HIF‐1α) and vascular endothelial growth factor (VEGF) in RPE cells with or without rapamycin under normoxic and hypoxic conditions using real‐time PCR and Western blot. We found that hypoxia increased the levels of mTOR, HIF‐1α, and VEGF. The suppression of HIF‐1α and VEGF by rapamycin was associated with dephosphorylation of mTOR and the downstream effector ribosomal protein S6 kinase (P70S6K) and 4E‐binding protein‐1 (4E‐BP1) of mTORC1. Rapamycin only inhibited the protein levels and did not change the mRNA expression of HIF‐1α. No cytotoxicity to the RPE cells by rapamycin was caused under either normoxia or hypoxia. Our data suggest that rapamycin suppresses hypoxia‐induced RPE cell proliferation through a mechanism related to the targeting of mTOR/HIF‐1α/VEGF signaling. Rapamycin may potentially provide a safe and effective novel treatment for choroidal vascular disease. © 2015 IUBMB Life, 67(6):446–452, 2015</jats:p> |
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| author | Liu, Ning‐Ning, Zhao, Ning, Cai, Na |
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| description | <jats:title>Abstract</jats:title><jats:p>Rapamycin, a highly specific inhibitor of mammalian target of rapamycin (mTOR), exhibits significant antitumor/antiangiogenic activity in human cancer cells. Its effect on the retinal pigment epithelial (RPE) cells was rarely investigated. This study assessed the proliferation of hypoxia‐induced RPE and the inhibitory effects of rapamycin using 3‐(4,5‐dimethylthazol‐2‐yl)−2,5‐diphenyltetrazolium bromide (MTT) assay and examined the expression of hypoxia‐inducible factor‐1α (HIF‐1α) and vascular endothelial growth factor (VEGF) in RPE cells with or without rapamycin under normoxic and hypoxic conditions using real‐time PCR and Western blot. We found that hypoxia increased the levels of mTOR, HIF‐1α, and VEGF. The suppression of HIF‐1α and VEGF by rapamycin was associated with dephosphorylation of mTOR and the downstream effector ribosomal protein S6 kinase (P70S6K) and 4E‐binding protein‐1 (4E‐BP1) of mTORC1. Rapamycin only inhibited the protein levels and did not change the mRNA expression of HIF‐1α. No cytotoxicity to the RPE cells by rapamycin was caused under either normoxia or hypoxia. Our data suggest that rapamycin suppresses hypoxia‐induced RPE cell proliferation through a mechanism related to the targeting of mTOR/HIF‐1α/VEGF signaling. Rapamycin may potentially provide a safe and effective novel treatment for choroidal vascular disease. © 2015 IUBMB Life, 67(6):446–452, 2015</jats:p> |
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| institution | DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Zi4, DE-Gla1, DE-15, DE-Pl11, DE-Rs1, DE-14, DE-105, DE-Ch1, DE-L229 |
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| spelling | Liu, Ning‐Ning Zhao, Ning Cai, Na 1521-6543 1521-6551 Wiley Cell Biology Clinical Biochemistry Genetics Molecular Biology Biochemistry http://dx.doi.org/10.1002/iub.1382 <jats:title>Abstract</jats:title><jats:p>Rapamycin, a highly specific inhibitor of mammalian target of rapamycin (mTOR), exhibits significant antitumor/antiangiogenic activity in human cancer cells. Its effect on the retinal pigment epithelial (RPE) cells was rarely investigated. This study assessed the proliferation of hypoxia‐induced RPE and the inhibitory effects of rapamycin using 3‐(4,5‐dimethylthazol‐2‐yl)−2,5‐diphenyltetrazolium bromide (MTT) assay and examined the expression of hypoxia‐inducible factor‐1α (HIF‐1α) and vascular endothelial growth factor (VEGF) in RPE cells with or without rapamycin under normoxic and hypoxic conditions using real‐time PCR and Western blot. We found that hypoxia increased the levels of mTOR, HIF‐1α, and VEGF. The suppression of HIF‐1α and VEGF by rapamycin was associated with dephosphorylation of mTOR and the downstream effector ribosomal protein S6 kinase (P70S6K) and 4E‐binding protein‐1 (4E‐BP1) of mTORC1. Rapamycin only inhibited the protein levels and did not change the mRNA expression of HIF‐1α. No cytotoxicity to the RPE cells by rapamycin was caused under either normoxia or hypoxia. Our data suggest that rapamycin suppresses hypoxia‐induced RPE cell proliferation through a mechanism related to the targeting of mTOR/HIF‐1α/VEGF signaling. Rapamycin may potentially provide a safe and effective novel treatment for choroidal vascular disease. © 2015 IUBMB Life, 67(6):446–452, 2015</jats:p> Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the <scp>/</scp>mTOR/HIF‐1α/VEGF<scp>/</scp> signaling IUBMB Life |
| spellingShingle | Liu, Ning‐Ning, Zhao, Ning, Cai, Na, IUBMB Life, Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling, Cell Biology, Clinical Biochemistry, Genetics, Molecular Biology, Biochemistry |
| title | Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_full | Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_fullStr | Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_full_unstemmed | Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_short | Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| title_sort | suppression of the proliferation of hypoxia‐induced retinal pigment epithelial cell by rapamycin through the <scp>scp>mtor/hif‐1α/vegf<scp>scp> signaling |
| title_unstemmed | Suppression of the proliferation of hypoxia‐Induced retinal pigment epithelial cell by rapamycin through the /mTOR/HIF‐1α/VEGF/ signaling |
| topic | Cell Biology, Clinical Biochemistry, Genetics, Molecular Biology, Biochemistry |
| url | http://dx.doi.org/10.1002/iub.1382 |