Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor
Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Tan, Lili [verfasserIn] Meng, Liang [verfasserIn] Shi, Xiaojing [verfasserIn] Yu, Bo [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Biotechnology letters - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1979, 39(2017), 7 vom: 03. Apr., Seite 967-976 |
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| Übergeordnetes Werk: |
volume:39 ; year:2017 ; number:7 ; day:03 ; month:04 ; pages:967-976 |
| Links: |
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| DOI / URN: |
10.1007/s10529-017-2337-y |
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| Katalog-ID: |
SPR010867686 |
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| 100 | 1 | |a Tan, Lili |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor |
| 264 | 1 | |c 2017 | |
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| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 520 | |a Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. | ||
| 650 | 4 | |a Atherosclerosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a MicroRNA-17-5p |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Proprotein convertase subtilisin kexin 9 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Very low density lipoprotein receptor |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Meng, Liang |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Xiaojing |e verfasserin |4 aut | |
| 700 | 1 | |a Yu, Bo |e verfasserin |4 aut | |
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| 912 | |a GBV_ILN_2014 | ||
| 912 | |a GBV_ILN_2015 | ||
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| 912 | |a GBV_ILN_2021 | ||
| 912 | |a GBV_ILN_2025 | ||
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| 912 | |a GBV_ILN_2027 | ||
| 912 | |a GBV_ILN_2031 | ||
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| 912 | |a GBV_ILN_2038 | ||
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| 912 | |a GBV_ILN_2044 | ||
| 912 | |a GBV_ILN_2048 | ||
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| 912 | |a GBV_ILN_2050 | ||
| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2065 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2070 | ||
| 912 | |a GBV_ILN_2086 | ||
| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2093 | ||
| 912 | |a GBV_ILN_2106 | ||
| 912 | |a GBV_ILN_2107 | ||
| 912 | |a GBV_ILN_2108 | ||
| 912 | |a GBV_ILN_2110 | ||
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| 912 | |a GBV_ILN_2112 | ||
| 912 | |a GBV_ILN_2113 | ||
| 912 | |a GBV_ILN_2116 | ||
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| 912 | |a GBV_ILN_4126 | ||
| 912 | |a GBV_ILN_4242 | ||
| 912 | |a GBV_ILN_4246 | ||
| 912 | |a GBV_ILN_4249 | ||
| 912 | |a GBV_ILN_4251 | ||
| 912 | |a GBV_ILN_4305 | ||
| 912 | |a GBV_ILN_4306 | ||
| 912 | |a GBV_ILN_4307 | ||
| 912 | |a GBV_ILN_4313 | ||
| 912 | |a GBV_ILN_4322 | ||
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| 912 | |a GBV_ILN_4324 | ||
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10.1007/s10529-017-2337-y doi (DE-627)SPR010867686 (SPR)s10529-017-2337-y-e DE-627 ger DE-627 rakwb eng 660 ASE 42.30 bkl 58.30 bkl Tan, Lili verfasserin aut Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. Atherosclerosis (dpeaa)DE-He213 MicroRNA-17-5p (dpeaa)DE-He213 Proprotein convertase subtilisin kexin 9 (dpeaa)DE-He213 Very low density lipoprotein receptor (dpeaa)DE-He213 Meng, Liang verfasserin aut Shi, Xiaojing verfasserin aut Yu, Bo verfasserin aut Enthalten in Biotechnology letters Dordrecht [u.a.] : Springer Science + Business Media B.V, 1979 39(2017), 7 vom: 03. Apr., Seite 967-976 (DE-627)312808356 (DE-600)2012203-2 1573-6776 nnns volume:39 year:2017 number:7 day:03 month:04 pages:967-976 https://dx.doi.org/10.1007/s10529-017-2337-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE 58.30 ASE AR 39 2017 7 03 04 967-976 |
| spelling |
10.1007/s10529-017-2337-y doi (DE-627)SPR010867686 (SPR)s10529-017-2337-y-e DE-627 ger DE-627 rakwb eng 660 ASE 42.30 bkl 58.30 bkl Tan, Lili verfasserin aut Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. Atherosclerosis (dpeaa)DE-He213 MicroRNA-17-5p (dpeaa)DE-He213 Proprotein convertase subtilisin kexin 9 (dpeaa)DE-He213 Very low density lipoprotein receptor (dpeaa)DE-He213 Meng, Liang verfasserin aut Shi, Xiaojing verfasserin aut Yu, Bo verfasserin aut Enthalten in Biotechnology letters Dordrecht [u.a.] : Springer Science + Business Media B.V, 1979 39(2017), 7 vom: 03. Apr., Seite 967-976 (DE-627)312808356 (DE-600)2012203-2 1573-6776 nnns volume:39 year:2017 number:7 day:03 month:04 pages:967-976 https://dx.doi.org/10.1007/s10529-017-2337-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE 58.30 ASE AR 39 2017 7 03 04 967-976 |
| allfields_unstemmed |
10.1007/s10529-017-2337-y doi (DE-627)SPR010867686 (SPR)s10529-017-2337-y-e DE-627 ger DE-627 rakwb eng 660 ASE 42.30 bkl 58.30 bkl Tan, Lili verfasserin aut Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. Atherosclerosis (dpeaa)DE-He213 MicroRNA-17-5p (dpeaa)DE-He213 Proprotein convertase subtilisin kexin 9 (dpeaa)DE-He213 Very low density lipoprotein receptor (dpeaa)DE-He213 Meng, Liang verfasserin aut Shi, Xiaojing verfasserin aut Yu, Bo verfasserin aut Enthalten in Biotechnology letters Dordrecht [u.a.] : Springer Science + Business Media B.V, 1979 39(2017), 7 vom: 03. Apr., Seite 967-976 (DE-627)312808356 (DE-600)2012203-2 1573-6776 nnns volume:39 year:2017 number:7 day:03 month:04 pages:967-976 https://dx.doi.org/10.1007/s10529-017-2337-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE 58.30 ASE AR 39 2017 7 03 04 967-976 |
| allfieldsGer |
10.1007/s10529-017-2337-y doi (DE-627)SPR010867686 (SPR)s10529-017-2337-y-e DE-627 ger DE-627 rakwb eng 660 ASE 42.30 bkl 58.30 bkl Tan, Lili verfasserin aut Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. Atherosclerosis (dpeaa)DE-He213 MicroRNA-17-5p (dpeaa)DE-He213 Proprotein convertase subtilisin kexin 9 (dpeaa)DE-He213 Very low density lipoprotein receptor (dpeaa)DE-He213 Meng, Liang verfasserin aut Shi, Xiaojing verfasserin aut Yu, Bo verfasserin aut Enthalten in Biotechnology letters Dordrecht [u.a.] : Springer Science + Business Media B.V, 1979 39(2017), 7 vom: 03. Apr., Seite 967-976 (DE-627)312808356 (DE-600)2012203-2 1573-6776 nnns volume:39 year:2017 number:7 day:03 month:04 pages:967-976 https://dx.doi.org/10.1007/s10529-017-2337-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE 58.30 ASE AR 39 2017 7 03 04 967-976 |
| allfieldsSound |
10.1007/s10529-017-2337-y doi (DE-627)SPR010867686 (SPR)s10529-017-2337-y-e DE-627 ger DE-627 rakwb eng 660 ASE 42.30 bkl 58.30 bkl Tan, Lili verfasserin aut Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. Atherosclerosis (dpeaa)DE-He213 MicroRNA-17-5p (dpeaa)DE-He213 Proprotein convertase subtilisin kexin 9 (dpeaa)DE-He213 Very low density lipoprotein receptor (dpeaa)DE-He213 Meng, Liang verfasserin aut Shi, Xiaojing verfasserin aut Yu, Bo verfasserin aut Enthalten in Biotechnology letters Dordrecht [u.a.] : Springer Science + Business Media B.V, 1979 39(2017), 7 vom: 03. Apr., Seite 967-976 (DE-627)312808356 (DE-600)2012203-2 1573-6776 nnns volume:39 year:2017 number:7 day:03 month:04 pages:967-976 https://dx.doi.org/10.1007/s10529-017-2337-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE 58.30 ASE AR 39 2017 7 03 04 967-976 |
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Enthalten in Biotechnology letters 39(2017), 7 vom: 03. Apr., Seite 967-976 volume:39 year:2017 number:7 day:03 month:04 pages:967-976 |
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Enthalten in Biotechnology letters 39(2017), 7 vom: 03. Apr., Seite 967-976 volume:39 year:2017 number:7 day:03 month:04 pages:967-976 |
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Atherosclerosis MicroRNA-17-5p Proprotein convertase subtilisin kexin 9 Very low density lipoprotein receptor |
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Biotechnology letters |
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Tan, Lili @@aut@@ Meng, Liang @@aut@@ Shi, Xiaojing @@aut@@ Yu, Bo @@aut@@ |
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Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. 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Tan, Lili |
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Tan, Lili ddc 660 bkl 42.30 bkl 58.30 misc Atherosclerosis misc MicroRNA-17-5p misc Proprotein convertase subtilisin kexin 9 misc Very low density lipoprotein receptor Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor |
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660 ASE 42.30 bkl 58.30 bkl Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor Atherosclerosis (dpeaa)DE-He213 MicroRNA-17-5p (dpeaa)DE-He213 Proprotein convertase subtilisin kexin 9 (dpeaa)DE-He213 Very low density lipoprotein receptor (dpeaa)DE-He213 |
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Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor |
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knockdown of microrna-17-5p ameliorates atherosclerotic lesions in $ apoe^{−/−} $ mice and restores the expression of very low density lipoprotein receptor |
| title_auth |
Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor |
| abstract |
Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. |
| abstractGer |
Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. |
| abstract_unstemmed |
Objective To propose and verify a hypothesis that miR-17-5p knockdown may mitigate atherosclerotic lesions using atherosclerotic $ ApoE^{−/−} $ mice as serum microRNA-17-5p (miR-17-5p) is elevated in patients with atherosclerosis. Results The level of miR-17-5p was higher while the level of very low density lipoprotein receptor (VLDLR), a predicted target of miR-17-5p, was lower in the peripheral blood lymphocytes (PBLs) of atherosclerosis patients as compared with control PBLs. $ ApoE^{−/−} $ mice fed with a high-cholesterol diet displayed marked atherosclerotic vascular lesions, which were ameliorated after treatment with antagomiR-17-5p. Moreover, the decreased VLDLR in atherosclerotic mice was partly restored when miR-17-5p was antagonized. Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs). In addition, the elevated expression of proprotein convertase subtilisin kexin 9 (PCSK9), a secreted protease that binds to and promotes VLDLR degradation, in the atherosclerotic mice was suppressed by antagomiR-17-5p. Conclusions A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS. |
| collection_details |
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| container_issue |
7 |
| title_short |
Knockdown of microRNA-17-5p ameliorates atherosclerotic lesions in $ ApoE^{−/−} $ mice and restores the expression of very low density lipoprotein receptor |
| url |
https://dx.doi.org/10.1007/s10529-017-2337-y |
| remote_bool |
true |
| author2 |
Meng, Liang Shi, Xiaojing Yu, Bo |
| author2Str |
Meng, Liang Shi, Xiaojing Yu, Bo |
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false |
| doi_str |
10.1007/s10529-017-2337-y |
| up_date |
2024-07-03T18:49:17.800Z |
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1803584859329789952 |
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| score |
7.398406 |