Sema3f Protects Against Subretinal Neovascularization In Vivo

Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema...
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Autor*in:	Ye Sun [verfasserIn] Raffael Liegl [verfasserIn] Yan Gong [verfasserIn] Anima Bühler [verfasserIn] Bertan Cakir [verfasserIn] Steven S. Meng [verfasserIn] Samuel B. Burnim [verfasserIn] Chi-Hsiu Liu [verfasserIn] Tristan Reuer [verfasserIn] Peipei Zhang [verfasserIn] Johanna M. Walz [verfasserIn] Franziska Ludwig [verfasserIn] Clemens Lange [verfasserIn] Hansjürgen Agostini [verfasserIn] Daniel Böhringer [verfasserIn] Günther Schlunck [verfasserIn] Lois E.H. Smith [verfasserIn] Andreas Stahl [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina

Übergeordnetes Werk:	In: EBioMedicine - Elsevier, 2015, 18(2017), C, Seite 281-287
Übergeordnetes Werk:	volume:18 ; year:2017 ; number:C ; pages:281-287

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.ebiom.2017.03.026

Katalog-ID:	DOAJ066275539

Internformat


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520			\|a Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization.
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allfields	10.1016/j.ebiom.2017.03.026 doi (DE-627)DOAJ066275539 (DE-599)DOAJc1aaf2f7dbd947aab178877a2b28334f DE-627 ger DE-627 rakwb eng R5-920 Ye Sun verfasserin aut Sema3f Protects Against Subretinal Neovascularization In Vivo 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization. AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina Medicine R Medicine (General) Raffael Liegl verfasserin aut Yan Gong verfasserin aut Anima Bühler verfasserin aut Bertan Cakir verfasserin aut Steven S. Meng verfasserin aut Samuel B. Burnim verfasserin aut Chi-Hsiu Liu verfasserin aut Tristan Reuer verfasserin aut Peipei Zhang verfasserin aut Johanna M. Walz verfasserin aut Franziska Ludwig verfasserin aut Clemens Lange verfasserin aut Hansjürgen Agostini verfasserin aut Daniel Böhringer verfasserin aut Günther Schlunck verfasserin aut Lois E.H. Smith verfasserin aut Andreas Stahl verfasserin aut In EBioMedicine Elsevier, 2015 18(2017), C, Seite 281-287 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:18 year:2017 number:C pages:281-287 https://doi.org/10.1016/j.ebiom.2017.03.026 kostenfrei https://doaj.org/article/c1aaf2f7dbd947aab178877a2b28334f kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396417301226 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 18 2017 C 281-287
spelling	10.1016/j.ebiom.2017.03.026 doi (DE-627)DOAJ066275539 (DE-599)DOAJc1aaf2f7dbd947aab178877a2b28334f DE-627 ger DE-627 rakwb eng R5-920 Ye Sun verfasserin aut Sema3f Protects Against Subretinal Neovascularization In Vivo 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization. AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina Medicine R Medicine (General) Raffael Liegl verfasserin aut Yan Gong verfasserin aut Anima Bühler verfasserin aut Bertan Cakir verfasserin aut Steven S. Meng verfasserin aut Samuel B. Burnim verfasserin aut Chi-Hsiu Liu verfasserin aut Tristan Reuer verfasserin aut Peipei Zhang verfasserin aut Johanna M. Walz verfasserin aut Franziska Ludwig verfasserin aut Clemens Lange verfasserin aut Hansjürgen Agostini verfasserin aut Daniel Böhringer verfasserin aut Günther Schlunck verfasserin aut Lois E.H. Smith verfasserin aut Andreas Stahl verfasserin aut In EBioMedicine Elsevier, 2015 18(2017), C, Seite 281-287 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:18 year:2017 number:C pages:281-287 https://doi.org/10.1016/j.ebiom.2017.03.026 kostenfrei https://doaj.org/article/c1aaf2f7dbd947aab178877a2b28334f kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396417301226 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 18 2017 C 281-287
allfields_unstemmed	10.1016/j.ebiom.2017.03.026 doi (DE-627)DOAJ066275539 (DE-599)DOAJc1aaf2f7dbd947aab178877a2b28334f DE-627 ger DE-627 rakwb eng R5-920 Ye Sun verfasserin aut Sema3f Protects Against Subretinal Neovascularization In Vivo 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization. AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina Medicine R Medicine (General) Raffael Liegl verfasserin aut Yan Gong verfasserin aut Anima Bühler verfasserin aut Bertan Cakir verfasserin aut Steven S. Meng verfasserin aut Samuel B. Burnim verfasserin aut Chi-Hsiu Liu verfasserin aut Tristan Reuer verfasserin aut Peipei Zhang verfasserin aut Johanna M. Walz verfasserin aut Franziska Ludwig verfasserin aut Clemens Lange verfasserin aut Hansjürgen Agostini verfasserin aut Daniel Böhringer verfasserin aut Günther Schlunck verfasserin aut Lois E.H. Smith verfasserin aut Andreas Stahl verfasserin aut In EBioMedicine Elsevier, 2015 18(2017), C, Seite 281-287 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:18 year:2017 number:C pages:281-287 https://doi.org/10.1016/j.ebiom.2017.03.026 kostenfrei https://doaj.org/article/c1aaf2f7dbd947aab178877a2b28334f kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396417301226 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 18 2017 C 281-287
allfieldsGer	10.1016/j.ebiom.2017.03.026 doi (DE-627)DOAJ066275539 (DE-599)DOAJc1aaf2f7dbd947aab178877a2b28334f DE-627 ger DE-627 rakwb eng R5-920 Ye Sun verfasserin aut Sema3f Protects Against Subretinal Neovascularization In Vivo 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization. AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina Medicine R Medicine (General) Raffael Liegl verfasserin aut Yan Gong verfasserin aut Anima Bühler verfasserin aut Bertan Cakir verfasserin aut Steven S. Meng verfasserin aut Samuel B. Burnim verfasserin aut Chi-Hsiu Liu verfasserin aut Tristan Reuer verfasserin aut Peipei Zhang verfasserin aut Johanna M. Walz verfasserin aut Franziska Ludwig verfasserin aut Clemens Lange verfasserin aut Hansjürgen Agostini verfasserin aut Daniel Böhringer verfasserin aut Günther Schlunck verfasserin aut Lois E.H. Smith verfasserin aut Andreas Stahl verfasserin aut In EBioMedicine Elsevier, 2015 18(2017), C, Seite 281-287 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:18 year:2017 number:C pages:281-287 https://doi.org/10.1016/j.ebiom.2017.03.026 kostenfrei https://doaj.org/article/c1aaf2f7dbd947aab178877a2b28334f kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396417301226 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 18 2017 C 281-287
allfieldsSound	10.1016/j.ebiom.2017.03.026 doi (DE-627)DOAJ066275539 (DE-599)DOAJc1aaf2f7dbd947aab178877a2b28334f DE-627 ger DE-627 rakwb eng R5-920 Ye Sun verfasserin aut Sema3f Protects Against Subretinal Neovascularization In Vivo 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization. AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina Medicine R Medicine (General) Raffael Liegl verfasserin aut Yan Gong verfasserin aut Anima Bühler verfasserin aut Bertan Cakir verfasserin aut Steven S. Meng verfasserin aut Samuel B. Burnim verfasserin aut Chi-Hsiu Liu verfasserin aut Tristan Reuer verfasserin aut Peipei Zhang verfasserin aut Johanna M. Walz verfasserin aut Franziska Ludwig verfasserin aut Clemens Lange verfasserin aut Hansjürgen Agostini verfasserin aut Daniel Böhringer verfasserin aut Günther Schlunck verfasserin aut Lois E.H. Smith verfasserin aut Andreas Stahl verfasserin aut In EBioMedicine Elsevier, 2015 18(2017), C, Seite 281-287 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:18 year:2017 number:C pages:281-287 https://doi.org/10.1016/j.ebiom.2017.03.026 kostenfrei https://doaj.org/article/c1aaf2f7dbd947aab178877a2b28334f kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396417301226 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 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_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 18 2017 C 281-287
language	English
source	In EBioMedicine 18(2017), C, Seite 281-287 volume:18 year:2017 number:C pages:281-287
sourceStr	In EBioMedicine 18(2017), C, Seite 281-287 volume:18 year:2017 number:C pages:281-287
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina Medicine R Medicine (General)
isfreeaccess_bool	true
container_title	EBioMedicine
authorswithroles_txt_mv	Ye Sun @@aut@@ Raffael Liegl @@aut@@ Yan Gong @@aut@@ Anima Bühler @@aut@@ Bertan Cakir @@aut@@ Steven S. Meng @@aut@@ Samuel B. Burnim @@aut@@ Chi-Hsiu Liu @@aut@@ Tristan Reuer @@aut@@ Peipei Zhang @@aut@@ Johanna M. Walz @@aut@@ Franziska Ludwig @@aut@@ Clemens Lange @@aut@@ Hansjürgen Agostini @@aut@@ Daniel Böhringer @@aut@@ Günther Schlunck @@aut@@ Lois E.H. Smith @@aut@@ Andreas Stahl @@aut@@
publishDateDaySort_date	2017-01-01T00:00:00Z
hierarchy_top_id	802540074
id	DOAJ066275539
language_de	englisch
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callnumber-first	R - Medicine
author	Ye Sun
spellingShingle	Ye Sun misc R5-920 misc AMD misc CNV misc RAP misc Laser-CNV misc Semaphorin misc Sema3f misc VLDLR misc Neovascularization misc Retina misc Medicine misc R misc Medicine (General) Sema3f Protects Against Subretinal Neovascularization In Vivo
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topic_title	R5-920 Sema3f Protects Against Subretinal Neovascularization In Vivo AMD CNV RAP Laser-CNV Semaphorin Sema3f VLDLR Neovascularization Retina
topic	misc R5-920 misc AMD misc CNV misc RAP misc Laser-CNV misc Semaphorin misc Sema3f misc VLDLR misc Neovascularization misc Retina misc Medicine misc R misc Medicine (General)
topic_unstemmed	misc R5-920 misc AMD misc CNV misc RAP misc Laser-CNV misc Semaphorin misc Sema3f misc VLDLR misc Neovascularization misc Retina misc Medicine misc R misc Medicine (General)
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title	Sema3f Protects Against Subretinal Neovascularization In Vivo
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title_sort	sema3f protects against subretinal neovascularization in vivo
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title_auth	Sema3f Protects Against Subretinal Neovascularization In Vivo
abstract	Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization.
abstractGer	Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization.
abstract_unstemmed	Pathological neovascularization of the outer retina is the hallmark of neovascular age-related macular degeneration (nAMD). Building on our previous observations that semaphorin 3F (Sema3f) is expressed in the outer retina and demonstrates anti-angiogenic potential, we have investigated whether Sema3f can be used to protect against subretinal neovascularization in two mouse models. Both in the very low-density lipid-receptor knockout (Vldlr−/−) model of spontaneous subretinal neovascularization as well as in the mouse model of laser-induced choroidal neovascularization (CNV), we found protective effects of Sema3f against the formation of pathologic neovascularization. In the Vldlr−/− model, AAV-induced overexpression of Sema3f reduced the size of pathologic neovascularization by 56%. In the laser-induced CNV model, intravitreally injected Sema3f reduced pathologic neovascularization by 30%. Combined, these results provide the first evidence from two distinct in vivo models for a use of Sema3f in protecting the outer retina against subretinal neovascularization.
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title_short	Sema3f Protects Against Subretinal Neovascularization In Vivo
url	https://doi.org/10.1016/j.ebiom.2017.03.026 https://doaj.org/article/c1aaf2f7dbd947aab178877a2b28334f http://www.sciencedirect.com/science/article/pii/S2352396417301226 https://doaj.org/toc/2352-3964
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