Proteomic analysis of cerebrospinal fluid of amyotrophic lateral sclerosis patients in the presence of autologous bone marrow derived mesenchymal stem cells

Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be in...

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Published inStem cell research & therapy Vol. 15; no. 1; pp. 301 - 18
Main Authors Reis, Ana Luiza Guimarães, Maximino, Jessica Ruivo, Lage, Luis Alberto de Padua Covas, Gomes, Hélio Rodrigues, Pereira, Juliana, Brofman, Paulo Roberto Slud, Senegaglia, Alexandra Cristina, Rebelatto, Carmen Lúcia Kuniyoshi, Daga, Debora Regina, Paiva, Wellingson Silva, Chadi, Gerson
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 15.09.2024
BioMed Central
BMC
Subjects
Adult
Aged
Amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis - cerebrospinal fluid
Amyotrophic Lateral Sclerosis - metabolism
Amyotrophic Lateral Sclerosis - therapy
Analysis
Apolipoprotein A-I - cerebrospinal fluid
Apolipoprotein A-I - metabolism
Apolipoproteins
Apolipoproteins E - cerebrospinal fluid
Apolipoproteins E - genetics
Apolipoproteins E - metabolism
Bone Marrow Cells - metabolism
Care and treatment
Cerebrospinal fluid
Development and progression
Female
Fibrin
Humans
Male
Mesenchymal Stem Cell Transplantation - methods
Mesenchymal stem cells
Mesenchymal Stem Cells - metabolism
Middle Aged
Protein Interaction Maps
Protein-protein interaction network
Protein-protein interactions
Proteomics
Proteomics - methods
Stem cells
Transplantation
Transplantation, Autologous
Amyotrophic lateral sclerosis
Protein-protein interaction network
Cerebrospinal fluid
Proteomics
Mesenchymal stem cells
Online AccessGet full text

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Abstract Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS. Using Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 × 10 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129. Proteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects. Extracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients. Clinicaltrial.gov identifier NCT0291768. Registered 28 September 2016.
AbstractList Background Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS. Method Using Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 x 10.sup.6 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129. Results Proteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects. Conclusions Extracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients. Trial registration Clinicaltrial.gov identifier NCT0291768. Registered 28 September 2016. Keywords: Amyotrophic lateral sclerosis, Mesenchymal stem cells, Proteomics, Protein-protein interaction network, Cerebrospinal fluid
Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS. Using Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 × 10 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129. Proteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects. Extracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients. Clinicaltrial.gov identifier NCT0291768. Registered 28 September 2016.
Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS. Using Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 x 10.sup.6 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129. Proteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects. Extracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients.
Abstract Background Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS. Method Using Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 × 106 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129. Results Proteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects. Conclusions Extracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients. Trial registration Clinicaltrial.gov identifier NCT0291768. Registered 28 September 2016.
Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS.BACKGROUNDAmyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease evolution or improving life quality of ALS patients. Thus, autologous stem cell therapy has emerged as an alternative treatment regime to be investigated in clinical ALS.Using Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 × 106 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129.METHODUsing Proteomics and Protein-Protein Interaction Network analyses combined with bioinformatics, the possible cellular mechanisms and molecular targets related to mesenchymal stem cells (MSCs, 1 × 106 cells/kg, intrathecally in the lumbar region of the spine) were investigated in cerebrospinal fluid (CSF) of ALS patients who received intrathecal infusions of autologous bone marrow-derived MSCs thirty days after cell therapy. Data are available via ProteomeXchange with identifier PXD053129.Proteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects.RESULTSProteomics revealed 220 deregulated proteins in CSF of ALS subjects treated with MSCs compared to CSF collected from the same patients prior to MSCs infusion. Bioinformatics enriched analyses highlighted events of Extracellular matrix and Cell adhesion molecules as well as related key targets APOA1, APOE, APP, C4A, C5, FGA, FGB, FGG and PLG in the CSF of cell treated ALS subjects.Extracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients.CONCLUSIONSExtracellular matrix and cell adhesion molecules as well as their related highlighted components have emerged as key targets of autologous MSCs in CSF of ALS patients.Clinicaltrial.gov identifier NCT0291768. Registered 28 September 2016.TRIAL REGISTRATIONClinicaltrial.gov identifier NCT0291768. Registered 28 September 2016.
ArticleNumber 301
Audience Academic
Author Senegaglia, Alexandra Cristina
Chadi, Gerson
Maximino, Jessica Ruivo
Rebelatto, Carmen Lúcia Kuniyoshi
Paiva, Wellingson Silva
Reis, Ana Luiza Guimarães
Brofman, Paulo Roberto Slud
Pereira, Juliana
Daga, Debora Regina
Lage, Luis Alberto de Padua Covas
Gomes, Hélio Rodrigues
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  surname: Chadi
  fullname: Chadi, Gerson
BackLink https://www.ncbi.nlm.nih.gov/pubmed/39278909$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Amyotrophic lateral sclerosis
Protein-protein interaction network
Cerebrospinal fluid
Proteomics
Mesenchymal stem cells
Language English
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Snippet Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing disease...
Background Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable of slowing...
Abstract Background Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressive motoneuron degenerative disorder. There are still no drugs capable...
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StartPage 301
SubjectTerms Adult
Aged
Amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis - cerebrospinal fluid
Amyotrophic Lateral Sclerosis - metabolism
Amyotrophic Lateral Sclerosis - therapy
Analysis
Apolipoprotein A-I - cerebrospinal fluid
Apolipoprotein A-I - metabolism
Apolipoproteins
Apolipoproteins E - cerebrospinal fluid
Apolipoproteins E - genetics
Apolipoproteins E - metabolism
Bone Marrow Cells - metabolism
Care and treatment
Cerebrospinal fluid
Development and progression
Female
Fibrin
Humans
Male
Mesenchymal Stem Cell Transplantation - methods
Mesenchymal stem cells
Mesenchymal Stem Cells - metabolism
Middle Aged
Protein Interaction Maps
Protein-protein interaction network
Protein-protein interactions
Proteomics
Proteomics - methods
Stem cells
Transplantation
Transplantation, Autologous
Title Proteomic analysis of cerebrospinal fluid of amyotrophic lateral sclerosis patients in the presence of autologous bone marrow derived mesenchymal stem cells
URI https://www.ncbi.nlm.nih.gov/pubmed/39278909
https://www.proquest.com/docview/3105491096
https://pubmed.ncbi.nlm.nih.gov/PMC11403799
https://doaj.org/article/15b73e097e494ce6b2633b7b2d896a55
Volume 15
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