Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice
Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippo...
Ausführliche Beschreibung
Autor*in: |
Wang, Jiapeng [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Anmerkung: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022 |
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Übergeordnetes Werk: |
Enthalten in: Translational stroke research - Berlin : Springer, 2010, 13(2022), 5 vom: 11. Feb., Seite 830-844 |
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Übergeordnetes Werk: |
volume:13 ; year:2022 ; number:5 ; day:11 ; month:02 ; pages:830-844 |
Links: |
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DOI / URN: |
10.1007/s12975-022-00994-w |
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Katalog-ID: |
SPR047890134 |
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520 | |a Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. | ||
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10.1007/s12975-022-00994-w doi (DE-627)SPR047890134 (SPR)s12975-022-00994-w-e DE-627 ger DE-627 rakwb eng Wang, Jiapeng verfasserin aut Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice 2022 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 2022 Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. Stroke (dpeaa)DE-He213 Neurogenesis (dpeaa)DE-He213 Sonic hedgehog (dpeaa)DE-He213 Smoothened (dpeaa)DE-He213 Behavior (dpeaa)DE-He213 Ware, Kierra aut Bedolla, Alicia aut Allgire, Emily aut Turcato, Flavia Correa aut Weed, Maxwell aut Sah, Renu aut Luo, Yu (orcid)0000-0002-7939-5505 aut Enthalten in Translational stroke research Berlin : Springer, 2010 13(2022), 5 vom: 11. Feb., Seite 830-844 (DE-627)620147210 (DE-600)2541897-X 1868-601X nnns volume:13 year:2022 number:5 day:11 month:02 pages:830-844 https://dx.doi.org/10.1007/s12975-022-00994-w 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_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_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_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 13 2022 5 11 02 830-844 |
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10.1007/s12975-022-00994-w doi (DE-627)SPR047890134 (SPR)s12975-022-00994-w-e DE-627 ger DE-627 rakwb eng Wang, Jiapeng verfasserin aut Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice 2022 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 2022 Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. Stroke (dpeaa)DE-He213 Neurogenesis (dpeaa)DE-He213 Sonic hedgehog (dpeaa)DE-He213 Smoothened (dpeaa)DE-He213 Behavior (dpeaa)DE-He213 Ware, Kierra aut Bedolla, Alicia aut Allgire, Emily aut Turcato, Flavia Correa aut Weed, Maxwell aut Sah, Renu aut Luo, Yu (orcid)0000-0002-7939-5505 aut Enthalten in Translational stroke research Berlin : Springer, 2010 13(2022), 5 vom: 11. Feb., Seite 830-844 (DE-627)620147210 (DE-600)2541897-X 1868-601X nnns volume:13 year:2022 number:5 day:11 month:02 pages:830-844 https://dx.doi.org/10.1007/s12975-022-00994-w 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_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_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_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 13 2022 5 11 02 830-844 |
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10.1007/s12975-022-00994-w doi (DE-627)SPR047890134 (SPR)s12975-022-00994-w-e DE-627 ger DE-627 rakwb eng Wang, Jiapeng verfasserin aut Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice 2022 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 2022 Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. Stroke (dpeaa)DE-He213 Neurogenesis (dpeaa)DE-He213 Sonic hedgehog (dpeaa)DE-He213 Smoothened (dpeaa)DE-He213 Behavior (dpeaa)DE-He213 Ware, Kierra aut Bedolla, Alicia aut Allgire, Emily aut Turcato, Flavia Correa aut Weed, Maxwell aut Sah, Renu aut Luo, Yu (orcid)0000-0002-7939-5505 aut Enthalten in Translational stroke research Berlin : Springer, 2010 13(2022), 5 vom: 11. Feb., Seite 830-844 (DE-627)620147210 (DE-600)2541897-X 1868-601X nnns volume:13 year:2022 number:5 day:11 month:02 pages:830-844 https://dx.doi.org/10.1007/s12975-022-00994-w 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_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_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_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 13 2022 5 11 02 830-844 |
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10.1007/s12975-022-00994-w doi (DE-627)SPR047890134 (SPR)s12975-022-00994-w-e DE-627 ger DE-627 rakwb eng Wang, Jiapeng verfasserin aut Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice 2022 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 2022 Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. Stroke (dpeaa)DE-He213 Neurogenesis (dpeaa)DE-He213 Sonic hedgehog (dpeaa)DE-He213 Smoothened (dpeaa)DE-He213 Behavior (dpeaa)DE-He213 Ware, Kierra aut Bedolla, Alicia aut Allgire, Emily aut Turcato, Flavia Correa aut Weed, Maxwell aut Sah, Renu aut Luo, Yu (orcid)0000-0002-7939-5505 aut Enthalten in Translational stroke research Berlin : Springer, 2010 13(2022), 5 vom: 11. Feb., Seite 830-844 (DE-627)620147210 (DE-600)2541897-X 1868-601X nnns volume:13 year:2022 number:5 day:11 month:02 pages:830-844 https://dx.doi.org/10.1007/s12975-022-00994-w 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_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_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_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 13 2022 5 11 02 830-844 |
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10.1007/s12975-022-00994-w doi (DE-627)SPR047890134 (SPR)s12975-022-00994-w-e DE-627 ger DE-627 rakwb eng Wang, Jiapeng verfasserin aut Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice 2022 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 2022 Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. Stroke (dpeaa)DE-He213 Neurogenesis (dpeaa)DE-He213 Sonic hedgehog (dpeaa)DE-He213 Smoothened (dpeaa)DE-He213 Behavior (dpeaa)DE-He213 Ware, Kierra aut Bedolla, Alicia aut Allgire, Emily aut Turcato, Flavia Correa aut Weed, Maxwell aut Sah, Renu aut Luo, Yu (orcid)0000-0002-7939-5505 aut Enthalten in Translational stroke research Berlin : Springer, 2010 13(2022), 5 vom: 11. Feb., Seite 830-844 (DE-627)620147210 (DE-600)2541897-X 1868-601X nnns volume:13 year:2022 number:5 day:11 month:02 pages:830-844 https://dx.doi.org/10.1007/s12975-022-00994-w 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_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_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_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 13 2022 5 11 02 830-844 |
language |
English |
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Enthalten in Translational stroke research 13(2022), 5 vom: 11. Feb., Seite 830-844 volume:13 year:2022 number:5 day:11 month:02 pages:830-844 |
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Enthalten in Translational stroke research 13(2022), 5 vom: 11. Feb., Seite 830-844 volume:13 year:2022 number:5 day:11 month:02 pages:830-844 |
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topic_facet |
Stroke Neurogenesis Sonic hedgehog Smoothened Behavior |
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Translational stroke research |
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Wang, Jiapeng @@aut@@ Ware, Kierra @@aut@@ Bedolla, Alicia @@aut@@ Allgire, Emily @@aut@@ Turcato, Flavia Correa @@aut@@ Weed, Maxwell @@aut@@ Sah, Renu @@aut@@ Luo, Yu @@aut@@ |
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However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. 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|
author |
Wang, Jiapeng |
spellingShingle |
Wang, Jiapeng misc Stroke misc Neurogenesis misc Sonic hedgehog misc Smoothened misc Behavior Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice |
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Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice Stroke (dpeaa)DE-He213 Neurogenesis (dpeaa)DE-He213 Sonic hedgehog (dpeaa)DE-He213 Smoothened (dpeaa)DE-He213 Behavior (dpeaa)DE-He213 |
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misc Stroke misc Neurogenesis misc Sonic hedgehog misc Smoothened misc Behavior |
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Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice |
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Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice |
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Wang, Jiapeng Ware, Kierra Bedolla, Alicia Allgire, Emily Turcato, Flavia Correa Weed, Maxwell Sah, Renu Luo, Yu |
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title_sort |
disruption of sonic hedgehog signaling accelerates age-related neurogenesis decline and abolishes stroke-induced neurogenesis and leads to increased anxiety behavior in stroke mice |
title_auth |
Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice |
abstract |
Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022 |
abstractGer |
Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022 |
abstract_unstemmed |
Abstract Sonic Hedgehog (SHH) signaling has a critical role in mediating developmental neurogenesis and has been implicated in adult subventricular (SVZ) neurogenesis. However, the precise role of Smoothened (SMO) receptor–mediated SHH signaling in adult neurogenesis during aging especially in hippocampal subgranular zone (SGZ) neurogenesis remains undefined. Additionally, our previous study showed that stimulation of SHH signaling post-stroke leads to increased neurogenesis and improved behavioral functions after stroke. However, it is not clear whether SHH signaling in neural stem cells (NSCs) is required for stroke-induced neurogenesis and functional recovery post-stroke. In this study, using conditional knockout (cKO) of SHH signaling receptor Smo gene in NSCs, we show a decreased neurogenesis at both SVZ and SGZ in young-adult mice and an accelerated depletion of neurogenic cells in the process of aging suggesting that SHH signaling is critical in maintaining neurogenesis during aging. Behavior studies revealed that compromised neurogenesis in Smo cKO mice leads to increased anxiety/depression-like behaviors without affecting general locomotor function or spatial and fear-related learning. Importantly, we also show that NSCs with a cKO of SHH signaling abolishes stroke-induced neurogenesis in Smo cKO mice. Compared to control mice, Smo cKO mice also show delayed motor function recovery and increased anxiety level after stroke. Our data highlights the essential role of Smo function in regulating adult neurogenesis and emotional behaviors during both aging and CNS injury such as stroke. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022 |
collection_details |
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container_issue |
5 |
title_short |
Disruption of Sonic Hedgehog Signaling Accelerates Age-Related Neurogenesis Decline and Abolishes Stroke-Induced Neurogenesis and Leads to Increased Anxiety Behavior in Stroke Mice |
url |
https://dx.doi.org/10.1007/s12975-022-00994-w |
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Ware, Kierra Bedolla, Alicia Allgire, Emily Turcato, Flavia Correa Weed, Maxwell Sah, Renu Luo, Yu |
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up_date |
2024-07-03T15:40:42.034Z |
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score |
7.3996916 |