Ataxia telangiectasia alters the ApoB and reelin pathway
Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response...
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| Autor*in: |
Canet-Pons, Júlia [verfasserIn] Schubert, Ralf [verfasserIn] Duecker, Ruth Pia [verfasserIn] Schrewe, Roland [verfasserIn] Wölke, Sandra [verfasserIn] Kieslich, Matthias [verfasserIn] Schnölzer, Martina [verfasserIn] Chiocchetti, Andreas [verfasserIn] Auburger, Georg [verfasserIn] Zielen, Stefan [verfasserIn] Warnken, Uwe [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Neurogenetics - Springer-Verlag, 2001, 19(2018), 4 vom: 21. Okt., Seite 237-255 |
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| Übergeordnetes Werk: |
volume:19 ; year:2018 ; number:4 ; day:21 ; month:10 ; pages:237-255 |
| Links: |
|---|
| DOI / URN: |
10.1007/s10048-018-0557-5 |
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| 520 | |a Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. | ||
| 650 | 4 | |a Ataxia telangiectasia |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Label-free mass spectrometry |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Diagnostic biomarkers |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Reelin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ApoB |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Schubert, Ralf |e verfasserin |4 aut | |
| 700 | 1 | |a Duecker, Ruth Pia |e verfasserin |4 aut | |
| 700 | 1 | |a Schrewe, Roland |e verfasserin |4 aut | |
| 700 | 1 | |a Wölke, Sandra |e verfasserin |4 aut | |
| 700 | 1 | |a Kieslich, Matthias |e verfasserin |4 aut | |
| 700 | 1 | |a Schnölzer, Martina |e verfasserin |4 aut | |
| 700 | 1 | |a Chiocchetti, Andreas |e verfasserin |4 aut | |
| 700 | 1 | |a Auburger, Georg |e verfasserin |4 aut | |
| 700 | 1 | |a Zielen, Stefan |e verfasserin |4 aut | |
| 700 | 1 | |a Warnken, Uwe |e verfasserin |4 aut | |
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10.1007/s10048-018-0557-5 doi (DE-627)SPR008235384 (SPR)s10048-018-0557-5-e DE-627 ger DE-627 rakwb eng Canet-Pons, Júlia verfasserin aut Ataxia telangiectasia alters the ApoB and reelin pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. Ataxia telangiectasia (dpeaa)DE-He213 Label-free mass spectrometry (dpeaa)DE-He213 Diagnostic biomarkers (dpeaa)DE-He213 Reelin (dpeaa)DE-He213 ApoB (dpeaa)DE-He213 Schubert, Ralf verfasserin aut Duecker, Ruth Pia verfasserin aut Schrewe, Roland verfasserin aut Wölke, Sandra verfasserin aut Kieslich, Matthias verfasserin aut Schnölzer, Martina verfasserin aut Chiocchetti, Andreas verfasserin aut Auburger, Georg verfasserin aut Zielen, Stefan verfasserin aut Warnken, Uwe verfasserin aut Enthalten in Neurogenetics Springer-Verlag, 2001 19(2018), 4 vom: 21. Okt., Seite 237-255 (DE-627)SPR00822823X nnns volume:19 year:2018 number:4 day:21 month:10 pages:237-255 https://dx.doi.org/10.1007/s10048-018-0557-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 19 2018 4 21 10 237-255 |
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10.1007/s10048-018-0557-5 doi (DE-627)SPR008235384 (SPR)s10048-018-0557-5-e DE-627 ger DE-627 rakwb eng Canet-Pons, Júlia verfasserin aut Ataxia telangiectasia alters the ApoB and reelin pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. Ataxia telangiectasia (dpeaa)DE-He213 Label-free mass spectrometry (dpeaa)DE-He213 Diagnostic biomarkers (dpeaa)DE-He213 Reelin (dpeaa)DE-He213 ApoB (dpeaa)DE-He213 Schubert, Ralf verfasserin aut Duecker, Ruth Pia verfasserin aut Schrewe, Roland verfasserin aut Wölke, Sandra verfasserin aut Kieslich, Matthias verfasserin aut Schnölzer, Martina verfasserin aut Chiocchetti, Andreas verfasserin aut Auburger, Georg verfasserin aut Zielen, Stefan verfasserin aut Warnken, Uwe verfasserin aut Enthalten in Neurogenetics Springer-Verlag, 2001 19(2018), 4 vom: 21. Okt., Seite 237-255 (DE-627)SPR00822823X nnns volume:19 year:2018 number:4 day:21 month:10 pages:237-255 https://dx.doi.org/10.1007/s10048-018-0557-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 19 2018 4 21 10 237-255 |
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10.1007/s10048-018-0557-5 doi (DE-627)SPR008235384 (SPR)s10048-018-0557-5-e DE-627 ger DE-627 rakwb eng Canet-Pons, Júlia verfasserin aut Ataxia telangiectasia alters the ApoB and reelin pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. Ataxia telangiectasia (dpeaa)DE-He213 Label-free mass spectrometry (dpeaa)DE-He213 Diagnostic biomarkers (dpeaa)DE-He213 Reelin (dpeaa)DE-He213 ApoB (dpeaa)DE-He213 Schubert, Ralf verfasserin aut Duecker, Ruth Pia verfasserin aut Schrewe, Roland verfasserin aut Wölke, Sandra verfasserin aut Kieslich, Matthias verfasserin aut Schnölzer, Martina verfasserin aut Chiocchetti, Andreas verfasserin aut Auburger, Georg verfasserin aut Zielen, Stefan verfasserin aut Warnken, Uwe verfasserin aut Enthalten in Neurogenetics Springer-Verlag, 2001 19(2018), 4 vom: 21. Okt., Seite 237-255 (DE-627)SPR00822823X nnns volume:19 year:2018 number:4 day:21 month:10 pages:237-255 https://dx.doi.org/10.1007/s10048-018-0557-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 19 2018 4 21 10 237-255 |
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10.1007/s10048-018-0557-5 doi (DE-627)SPR008235384 (SPR)s10048-018-0557-5-e DE-627 ger DE-627 rakwb eng Canet-Pons, Júlia verfasserin aut Ataxia telangiectasia alters the ApoB and reelin pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. Ataxia telangiectasia (dpeaa)DE-He213 Label-free mass spectrometry (dpeaa)DE-He213 Diagnostic biomarkers (dpeaa)DE-He213 Reelin (dpeaa)DE-He213 ApoB (dpeaa)DE-He213 Schubert, Ralf verfasserin aut Duecker, Ruth Pia verfasserin aut Schrewe, Roland verfasserin aut Wölke, Sandra verfasserin aut Kieslich, Matthias verfasserin aut Schnölzer, Martina verfasserin aut Chiocchetti, Andreas verfasserin aut Auburger, Georg verfasserin aut Zielen, Stefan verfasserin aut Warnken, Uwe verfasserin aut Enthalten in Neurogenetics Springer-Verlag, 2001 19(2018), 4 vom: 21. Okt., Seite 237-255 (DE-627)SPR00822823X nnns volume:19 year:2018 number:4 day:21 month:10 pages:237-255 https://dx.doi.org/10.1007/s10048-018-0557-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 19 2018 4 21 10 237-255 |
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10.1007/s10048-018-0557-5 doi (DE-627)SPR008235384 (SPR)s10048-018-0557-5-e DE-627 ger DE-627 rakwb eng Canet-Pons, Júlia verfasserin aut Ataxia telangiectasia alters the ApoB and reelin pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. Ataxia telangiectasia (dpeaa)DE-He213 Label-free mass spectrometry (dpeaa)DE-He213 Diagnostic biomarkers (dpeaa)DE-He213 Reelin (dpeaa)DE-He213 ApoB (dpeaa)DE-He213 Schubert, Ralf verfasserin aut Duecker, Ruth Pia verfasserin aut Schrewe, Roland verfasserin aut Wölke, Sandra verfasserin aut Kieslich, Matthias verfasserin aut Schnölzer, Martina verfasserin aut Chiocchetti, Andreas verfasserin aut Auburger, Georg verfasserin aut Zielen, Stefan verfasserin aut Warnken, Uwe verfasserin aut Enthalten in Neurogenetics Springer-Verlag, 2001 19(2018), 4 vom: 21. Okt., Seite 237-255 (DE-627)SPR00822823X nnns volume:19 year:2018 number:4 day:21 month:10 pages:237-255 https://dx.doi.org/10.1007/s10048-018-0557-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 19 2018 4 21 10 237-255 |
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Ataxia telangiectasia alters the ApoB and reelin pathway Ataxia telangiectasia (dpeaa)DE-He213 Label-free mass spectrometry (dpeaa)DE-He213 Diagnostic biomarkers (dpeaa)DE-He213 Reelin (dpeaa)DE-He213 ApoB (dpeaa)DE-He213 |
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Canet-Pons, Júlia Schubert, Ralf Duecker, Ruth Pia Schrewe, Roland Wölke, Sandra Kieslich, Matthias Schnölzer, Martina Chiocchetti, Andreas Auburger, Georg Zielen, Stefan Warnken, Uwe |
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ataxia telangiectasia alters the apob and reelin pathway |
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Ataxia telangiectasia alters the ApoB and reelin pathway |
| abstract |
Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. |
| abstractGer |
Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. |
| abstract_unstemmed |
Abstract Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood. Employing global proteomic profiling of cerebrospinal fluid from patients at ages around 15 years, we detected reduced calbindin, reelin, cerebellin-1, cerebellin-3, protocadherin fat 2, sempahorin 7A, and increased apolipoprotein B and J peptides. Bioinformatic enrichment was observed for pathways of lipoproteins, endocytosis, extracellular matrix receptor interaction, peptidase activity, adhesion, calcium binding, and complement immunity. This seemed important since secretion of reelin from glutamatergic afferent axons is crucial for PN lipoprotein receptor endocytosis and lipid signaling. Reelin expression is downregulated by irradiation and reelin/ApoB mutations are known causes of ataxia. Validation efforts in 2-month-old Atm−/− mice before onset of motor deficits confirmed cerebellar transcript reductions for reelin receptors Apoer2/Vldlr with increases for their ligands Apoe/Apoh and cholesterol 24-hydroxylase Cyp46a1. Concomitant dysregulations were found for Vglut2/Sema7a as climbing fiber markers, glutamate receptors like Grin2b, and calcium homeostasis factors (Atp2b2, Calb1, Itpr1), while factors involved in DNA damage, oxidative stress, neuroinflammation, and cell adhesion were normal at this stage. Quantitative immunoblots confirmed ApoB and ApoJ increases and VLDLR reduction in cerebellar tissue at the age of 2 months. These findings show that ApoB excess and reelin signaling deficits reflect the neurodegeneration in A-T in a sensitive and specific way. As extracellular factors, apolipoproteins and their cargo such as vitamin E may be useful for neuroprotective interventions. |
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