The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death

Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are availab...
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Autor*in:	Richard Younes [verfasserIn] Youssef Issa [verfasserIn] Nadia Jdaa [verfasserIn] Batoul Chouaib [verfasserIn] Véronique Brugioti [verfasserIn] Désiré Challuau [verfasserIn] Cédric Raoul [verfasserIn] Frédérique Scamps [verfasserIn] Frédéric Cuisinier [verfasserIn] Cécile Hilaire [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell

Übergeordnetes Werk:	In: Biomedicines - MDPI AG, 2014, 11(2023), 8, p 2152
Übergeordnetes Werk:	volume:11 ; year:2023 ; number:8, p 2152

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/biomedicines11082152

Katalog-ID:	DOAJ093647085

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520			\|a Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS.
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allfields	10.3390/biomedicines11082152 doi (DE-627)DOAJ093647085 (DE-599)DOAJbd5e80d3b152444d8948c698babc4e16 DE-627 ger DE-627 rakwb eng QH301-705.5 Richard Younes verfasserin aut The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS. amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell Biology (General) Youssef Issa verfasserin aut Nadia Jdaa verfasserin aut Batoul Chouaib verfasserin aut Véronique Brugioti verfasserin aut Désiré Challuau verfasserin aut Cédric Raoul verfasserin aut Frédérique Scamps verfasserin aut Frédéric Cuisinier verfasserin aut Cécile Hilaire verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 8, p 2152 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:8, p 2152 https://doi.org/10.3390/biomedicines11082152 kostenfrei https://doaj.org/article/bd5e80d3b152444d8948c698babc4e16 kostenfrei https://www.mdpi.com/2227-9059/11/8/2152 kostenfrei https://doaj.org/toc/2227-9059 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_70 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 8, p 2152
spelling	10.3390/biomedicines11082152 doi (DE-627)DOAJ093647085 (DE-599)DOAJbd5e80d3b152444d8948c698babc4e16 DE-627 ger DE-627 rakwb eng QH301-705.5 Richard Younes verfasserin aut The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS. amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell Biology (General) Youssef Issa verfasserin aut Nadia Jdaa verfasserin aut Batoul Chouaib verfasserin aut Véronique Brugioti verfasserin aut Désiré Challuau verfasserin aut Cédric Raoul verfasserin aut Frédérique Scamps verfasserin aut Frédéric Cuisinier verfasserin aut Cécile Hilaire verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 8, p 2152 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:8, p 2152 https://doi.org/10.3390/biomedicines11082152 kostenfrei https://doaj.org/article/bd5e80d3b152444d8948c698babc4e16 kostenfrei https://www.mdpi.com/2227-9059/11/8/2152 kostenfrei https://doaj.org/toc/2227-9059 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_70 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 8, p 2152
allfields_unstemmed	10.3390/biomedicines11082152 doi (DE-627)DOAJ093647085 (DE-599)DOAJbd5e80d3b152444d8948c698babc4e16 DE-627 ger DE-627 rakwb eng QH301-705.5 Richard Younes verfasserin aut The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS. amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell Biology (General) Youssef Issa verfasserin aut Nadia Jdaa verfasserin aut Batoul Chouaib verfasserin aut Véronique Brugioti verfasserin aut Désiré Challuau verfasserin aut Cédric Raoul verfasserin aut Frédérique Scamps verfasserin aut Frédéric Cuisinier verfasserin aut Cécile Hilaire verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 8, p 2152 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:8, p 2152 https://doi.org/10.3390/biomedicines11082152 kostenfrei https://doaj.org/article/bd5e80d3b152444d8948c698babc4e16 kostenfrei https://www.mdpi.com/2227-9059/11/8/2152 kostenfrei https://doaj.org/toc/2227-9059 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_70 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 8, p 2152
allfieldsGer	10.3390/biomedicines11082152 doi (DE-627)DOAJ093647085 (DE-599)DOAJbd5e80d3b152444d8948c698babc4e16 DE-627 ger DE-627 rakwb eng QH301-705.5 Richard Younes verfasserin aut The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS. amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell Biology (General) Youssef Issa verfasserin aut Nadia Jdaa verfasserin aut Batoul Chouaib verfasserin aut Véronique Brugioti verfasserin aut Désiré Challuau verfasserin aut Cédric Raoul verfasserin aut Frédérique Scamps verfasserin aut Frédéric Cuisinier verfasserin aut Cécile Hilaire verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 8, p 2152 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:8, p 2152 https://doi.org/10.3390/biomedicines11082152 kostenfrei https://doaj.org/article/bd5e80d3b152444d8948c698babc4e16 kostenfrei https://www.mdpi.com/2227-9059/11/8/2152 kostenfrei https://doaj.org/toc/2227-9059 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_70 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 8, p 2152
allfieldsSound	10.3390/biomedicines11082152 doi (DE-627)DOAJ093647085 (DE-599)DOAJbd5e80d3b152444d8948c698babc4e16 DE-627 ger DE-627 rakwb eng QH301-705.5 Richard Younes verfasserin aut The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS. amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell Biology (General) Youssef Issa verfasserin aut Nadia Jdaa verfasserin aut Batoul Chouaib verfasserin aut Véronique Brugioti verfasserin aut Désiré Challuau verfasserin aut Cédric Raoul verfasserin aut Frédérique Scamps verfasserin aut Frédéric Cuisinier verfasserin aut Cécile Hilaire verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 8, p 2152 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:8, p 2152 https://doi.org/10.3390/biomedicines11082152 kostenfrei https://doaj.org/article/bd5e80d3b152444d8948c698babc4e16 kostenfrei https://www.mdpi.com/2227-9059/11/8/2152 kostenfrei https://doaj.org/toc/2227-9059 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_70 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 8, p 2152
language	English
source	In Biomedicines 11(2023), 8, p 2152 volume:11 year:2023 number:8, p 2152
sourceStr	In Biomedicines 11(2023), 8, p 2152 volume:11 year:2023 number:8, p 2152
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell Biology (General)
isfreeaccess_bool	true
container_title	Biomedicines
authorswithroles_txt_mv	Richard Younes @@aut@@ Youssef Issa @@aut@@ Nadia Jdaa @@aut@@ Batoul Chouaib @@aut@@ Véronique Brugioti @@aut@@ Désiré Challuau @@aut@@ Cédric Raoul @@aut@@ Frédérique Scamps @@aut@@ Frédéric Cuisinier @@aut@@ Cécile Hilaire @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	750370483
id	DOAJ093647085
language_de	englisch
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callnumber-first	Q - Science
author	Richard Younes
spellingShingle	Richard Younes misc QH301-705.5 misc amyotrophic lateral sclerosis misc neuropathology misc death misc axon outgrowth misc electrical activity misc dental pulp stem cell misc Biology (General) The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death
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topic_title	QH301-705.5 The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death amyotrophic lateral sclerosis neuropathology death axon outgrowth electrical activity dental pulp stem cell
topic	misc QH301-705.5 misc amyotrophic lateral sclerosis misc neuropathology misc death misc axon outgrowth misc electrical activity misc dental pulp stem cell misc Biology (General)
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title	The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death
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title_full	The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death
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author_browse	Richard Younes Youssef Issa Nadia Jdaa Batoul Chouaib Véronique Brugioti Désiré Challuau Cédric Raoul Frédérique Scamps Frédéric Cuisinier Cécile Hilaire
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title_sort	secretome of human dental pulp stem cells and its components gdf15 and hb-egf protect amyotrophic lateral sclerosis motoneurons against death
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title_auth	The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death
abstract	Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS.
abstractGer	Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS.
abstract_unstemmed	Amyotrophic lateral sclerosis (ALS) is a fatal and incurable paralytic disorder caused by the progressive death of upper and lower motoneurons. Although numerous strategies have been developed to slow disease progression and improve life quality, to date only a few therapeutic treatments are available with still unsatisfactory therapeutic benefits. The secretome of dental pulp stem cells (DPSCs) contains numerous neurotrophic factors that could promote motoneuron survival. Accordingly, DPSCs confer neuroprotective benefits to the <i<SOD1<sup<G93A</sup<</i< mouse model of ALS. However, the mode of action of DPSC secretome on motoneurons remains largely unknown. Here, we used conditioned medium of human DPSCs (DPSCs-CM) and assessed its effect on survival, axonal length, and electrical activity of cultured wildtype and <i<SOD1<sup<G93A</sup<</i< motoneurons. To further understand the role of individual factors secreted by DPSCs and to circumvent the secretome variability bias, we focused on GDF15 and HB-EGF whose neuroprotective properties remain elusive in the ALS pathogenic context. DPSCs-CM rescues motoneurons from trophic factor deprivation-induced death, promotes axon outgrowth of wildtype but not <i<SOD1<sup<G93A</sup<</i< mutant motoneurons, and has no impact on the spontaneous electrical activity of wildtype or mutant motoneurons. Both GDF15 and HB-EGF protect <i<SOD1<sup<G93A</sup<</i< motoneurons against nitric oxide-induced death, but not against death induced by trophic factor deprivation. GDF15 and HB-EGF receptors were found to be expressed in the spinal cord, with a two-fold increase in expression for the GDF15 low-affinity receptor in <i<SOD1<sup<G93A</sup<</i< mice. Therefore, the secretome of DPSCs appears as a new potential therapeutic candidate for ALS.
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title_short	The Secretome of Human Dental Pulp Stem Cells and Its Components GDF15 and HB-EGF Protect Amyotrophic Lateral Sclerosis Motoneurons against Death
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