Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis

Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	He, Zhirong [verfasserIn] Zhao, Yanyan Zhu, Yongxia Wang, Weihua Liu, Xin Lu, Fen

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	TUG1 CI/R Inflammatory damage Apoptosis

Anmerkung:	© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021

Übergeordnetes Werk:	Enthalten in: Neurotoxicity research - New York, NY : Springer, 1999, 40(2021), 1 vom: 01. Dez., Seite 1-13
Übergeordnetes Werk:	volume:40 ; year:2021 ; number:1 ; day:01 ; month:12 ; pages:1-13

Links:	Volltext

DOI / URN:	10.1007/s12640-021-00446-7

Katalog-ID:	SPR04604339X

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245	1	0	\|a Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis
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520			\|a Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R.
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allfields	10.1007/s12640-021-00446-7 doi (DE-627)SPR04604339X (SPR)s12640-021-00446-7-e DE-627 ger DE-627 rakwb eng He, Zhirong verfasserin aut Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. TUG1 (dpeaa)DE-He213 CI/R (dpeaa)DE-He213 Inflammatory damage (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Zhao, Yanyan aut Zhu, Yongxia aut Wang, Weihua aut Liu, Xin aut Lu, Fen aut Enthalten in Neurotoxicity research New York, NY : Springer, 1999 40(2021), 1 vom: 01. Dez., Seite 1-13 (DE-627)345201094 (DE-600)2074876-0 1476-3524 nnns volume:40 year:2021 number:1 day:01 month:12 pages:1-13 https://dx.doi.org/10.1007/s12640-021-00446-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_101 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_206 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 40 2021 1 01 12 1-13
spelling	10.1007/s12640-021-00446-7 doi (DE-627)SPR04604339X (SPR)s12640-021-00446-7-e DE-627 ger DE-627 rakwb eng He, Zhirong verfasserin aut Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. TUG1 (dpeaa)DE-He213 CI/R (dpeaa)DE-He213 Inflammatory damage (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Zhao, Yanyan aut Zhu, Yongxia aut Wang, Weihua aut Liu, Xin aut Lu, Fen aut Enthalten in Neurotoxicity research New York, NY : Springer, 1999 40(2021), 1 vom: 01. Dez., Seite 1-13 (DE-627)345201094 (DE-600)2074876-0 1476-3524 nnns volume:40 year:2021 number:1 day:01 month:12 pages:1-13 https://dx.doi.org/10.1007/s12640-021-00446-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_101 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_206 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 40 2021 1 01 12 1-13
allfields_unstemmed	10.1007/s12640-021-00446-7 doi (DE-627)SPR04604339X (SPR)s12640-021-00446-7-e DE-627 ger DE-627 rakwb eng He, Zhirong verfasserin aut Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. TUG1 (dpeaa)DE-He213 CI/R (dpeaa)DE-He213 Inflammatory damage (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Zhao, Yanyan aut Zhu, Yongxia aut Wang, Weihua aut Liu, Xin aut Lu, Fen aut Enthalten in Neurotoxicity research New York, NY : Springer, 1999 40(2021), 1 vom: 01. Dez., Seite 1-13 (DE-627)345201094 (DE-600)2074876-0 1476-3524 nnns volume:40 year:2021 number:1 day:01 month:12 pages:1-13 https://dx.doi.org/10.1007/s12640-021-00446-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_101 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_206 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 40 2021 1 01 12 1-13
allfieldsGer	10.1007/s12640-021-00446-7 doi (DE-627)SPR04604339X (SPR)s12640-021-00446-7-e DE-627 ger DE-627 rakwb eng He, Zhirong verfasserin aut Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. TUG1 (dpeaa)DE-He213 CI/R (dpeaa)DE-He213 Inflammatory damage (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Zhao, Yanyan aut Zhu, Yongxia aut Wang, Weihua aut Liu, Xin aut Lu, Fen aut Enthalten in Neurotoxicity research New York, NY : Springer, 1999 40(2021), 1 vom: 01. Dez., Seite 1-13 (DE-627)345201094 (DE-600)2074876-0 1476-3524 nnns volume:40 year:2021 number:1 day:01 month:12 pages:1-13 https://dx.doi.org/10.1007/s12640-021-00446-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_101 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_206 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 40 2021 1 01 12 1-13
allfieldsSound	10.1007/s12640-021-00446-7 doi (DE-627)SPR04604339X (SPR)s12640-021-00446-7-e DE-627 ger DE-627 rakwb eng He, Zhirong verfasserin aut Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. TUG1 (dpeaa)DE-He213 CI/R (dpeaa)DE-He213 Inflammatory damage (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Zhao, Yanyan aut Zhu, Yongxia aut Wang, Weihua aut Liu, Xin aut Lu, Fen aut Enthalten in Neurotoxicity research New York, NY : Springer, 1999 40(2021), 1 vom: 01. Dez., Seite 1-13 (DE-627)345201094 (DE-600)2074876-0 1476-3524 nnns volume:40 year:2021 number:1 day:01 month:12 pages:1-13 https://dx.doi.org/10.1007/s12640-021-00446-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_101 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_206 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_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 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_2118 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 40 2021 1 01 12 1-13
language	English
source	Enthalten in Neurotoxicity research 40(2021), 1 vom: 01. Dez., Seite 1-13 volume:40 year:2021 number:1 day:01 month:12 pages:1-13
sourceStr	Enthalten in Neurotoxicity research 40(2021), 1 vom: 01. Dez., Seite 1-13 volume:40 year:2021 number:1 day:01 month:12 pages:1-13
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	TUG1 CI/R Inflammatory damage Apoptosis
isfreeaccess_bool	false
container_title	Neurotoxicity research
authorswithroles_txt_mv	He, Zhirong @@aut@@ Zhao, Yanyan @@aut@@ Zhu, Yongxia @@aut@@ Wang, Weihua @@aut@@ Liu, Xin @@aut@@ Lu, Fen @@aut@@
publishDateDaySort_date	2021-12-01T00:00:00Z
hierarchy_top_id	345201094
id	SPR04604339X
language_de	englisch
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However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. 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author	He, Zhirong
spellingShingle	He, Zhirong misc TUG1 misc CI/R misc Inflammatory damage misc Apoptosis Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis
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topic_title	Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis TUG1 (dpeaa)DE-He213 CI/R (dpeaa)DE-He213 Inflammatory damage (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213
topic	misc TUG1 misc CI/R misc Inflammatory damage misc Apoptosis
topic_unstemmed	misc TUG1 misc CI/R misc Inflammatory damage misc Apoptosis
topic_browse	misc TUG1 misc CI/R misc Inflammatory damage misc Apoptosis
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title	Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis
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title_full	Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis
author_sort	He, Zhirong
journal	Neurotoxicity research
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author_browse	He, Zhirong Zhao, Yanyan Zhu, Yongxia Wang, Weihua Liu, Xin Lu, Fen
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format_se	Elektronische Aufsätze
author-letter	He, Zhirong
doi_str_mv	10.1007/s12640-021-00446-7
title_sort	interfering tug1 attenuates cerebrovascular endothelial apoptosis and inflammatory injury after cerebral ischemia/reperfusion via tug1/mir-410/foxo3 cerna axis
title_auth	Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis
abstract	Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021
abstractGer	Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021
abstract_unstemmed	Abstract Background Emerging studies illustrate that long non-coding RNA TUG1 (TUG1) participates in neuron death after ischemia. However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. Blockage of TUG1 decreased infarct volume and increased neurological score in MCAO/R mice, accompanied with elevated Bcl-2 expression and declined expression of IL-1β, IL-6, TNF-α, Bax, and cleaved caspase 3. Abovementioned proteins were similarly expressed in OGD/R-induced BMECs with TUG1 knockdown, paralleled with diminished apoptosis rate. Either, miR-410 overexpression and FOXO3 interference could suppress OGD/R-induced inflammatory and apoptotic responses. Of note, TUG1 and FOXO3 are competing endogenous RNAs (ceRNAs) for miR-410 via target binding. Depleting miR-410 counteracted the role of TUG1 exhaustion, and reinforcing FOXO3 abated the effect of miR-410 overexpression. Conclusion Exhausting TUG1 could alleviate CI/R-induced inflammatory injury and apoptosis in brain tissues and BMECs via targeting miR-410/FOXO3 axis, suggesting an innovative perspective from cerebrovascular endothelial cells in the pathogenesis and treatment of CI/R. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021
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container_issue	1
title_short	Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis
url	https://dx.doi.org/10.1007/s12640-021-00446-7
remote_bool	true
author2	Zhao, Yanyan Zhu, Yongxia Wang, Weihua Liu, Xin Lu, Fen
author2Str	Zhao, Yanyan Zhu, Yongxia Wang, Weihua Liu, Xin Lu, Fen
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doi_str	10.1007/s12640-021-00446-7
up_date	2024-07-03T19:58:03.241Z
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However, the role of TUG1 in cerebral ischemia/reperfusion (CI/R) injury through cerebrovascular pathology was undetermined yet. Methods Expression of TUG1, miRNA-410-3p (miR-410), and forkhead box O3 (FOXO3) was detected by RT-qPCR and western blot. Neural function, apoptosis, and inflammatory damage were assessed by triphenyltetrazolium chloride straining, modified neurological severity score, fluorescence-activated cell sorting method, and western blot. The relationship among TUG1, miR-410, and FOXO3 was identified by dual-luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation. Results TUG1 was upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) mice and oxygen–glucose deprivation/reoxygenation (OGD/R)-induced mouse brain microvascular endothelial cells (BMECs) in a certain of time-dependent manner. 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Interfering TUG1 Attenuates Cerebrovascular Endothelial Apoptosis and Inflammatory injury After Cerebral Ischemia/Reperfusion via TUG1/miR-410/FOXO3 ceRNA Axis

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