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No proinflammatory signature in CD34+ hematopoietic progenitor cells in multiple sclerosis patients
A Lutterotti1,2
I Jelčić1,3
C Schulze4
S Schippling1
P Breiden1
B Mazzanti5
S Reinhardt1
M DiGioia5
A Repice6
L Massacesi6
A Sputtek7
G Salinas-Riester8
N Kroeger9
M Sospedra1
R Saccardi5
A Zander9
R Martin1,3
1Institute of Neuroimmunology and Clinical MS Research, Center for Molecular Neurobiology Hamburg, Germany
2Clinical Department of Neurology, Innsbruck Medical University, Austria
3Department of Neurology, University Hospital Zurich, Switzerland
4Systems Biology and Protein-Protein Interaction, Center for Molecular Neurobiology Hamburg, Germany
5Department of Haematology, Careggi University Hospital, Italy
6Department of Neurological Sciences, University of Florence, Italy
7Institute of Transfusion Medicine, University Medical Center Hamburg Eppendorf, Germany
8DNA Microarray Facility, University of Medicine Göttingen, Germany
9Center for Stem Cell Transplantation, University Medical Center Hamburg Eppendorf, Germany
Andreas Lutterotti, Clinical Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria
Abstract
Autologous hematopoietic stem cell transplantation (aHSCT) has been used as a therapeutic approach in multiple sclerosis (MS). However, it is still unclear if the immune system that emerges from autologous CD34+ hematopoietic progenitor cells (HPC) of MS patients is pre-conditioned to re-develop the proinflammatory phenotype. The objective of this article is to compare the whole genome gene and microRNA expression signature in CD34+ HPC of MS patients and healthy donors (HD). CD34+ HPC were isolated from peripheral blood of eight MS patients and five HD and analyzed by whole genome gene expression and microRNA expression microarray. Among the differentially expressed genes (DEGs) only TNNT1 reached statistical significance (logFC=3.1, p<0.01). The microRNA expression was not significantly different between MS patients and HD. We did not find significant alterations of gene expression or microRNA profiles in CD34+ HPCs of MS patients. Our results support the use of aHSCT for treatment of MS.
A Lutterotti1,2
I Jelčić1,3
C Schulze4
S Schippling1
P Breiden1
B Mazzanti5
S Reinhardt1
M DiGioia5
A Repice6
L Massacesi6
A Sputtek7
G Salinas-Riester8
N Kroeger9
M Sospedra1
R Saccardi5
A Zander9
R Martin1,3
1Institute of Neuroimmunology and Clinical MS Research, Center for Molecular Neurobiology Hamburg, Germany
2Clinical Department of Neurology, Innsbruck Medical University, Austria
3Department of Neurology, University Hospital Zurich, Switzerland
4Systems Biology and Protein-Protein Interaction, Center for Molecular Neurobiology Hamburg, Germany
5Department of Haematology, Careggi University Hospital, Italy
6Department of Neurological Sciences, University of Florence, Italy
7Institute of Transfusion Medicine, University Medical Center Hamburg Eppendorf, Germany
8DNA Microarray Facility, University of Medicine Göttingen, Germany
9Center for Stem Cell Transplantation, University Medical Center Hamburg Eppendorf, Germany
Andreas Lutterotti, Clinical Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria
Abstract
Autologous hematopoietic stem cell transplantation (aHSCT) has been used as a therapeutic approach in multiple sclerosis (MS). However, it is still unclear if the immune system that emerges from autologous CD34+ hematopoietic progenitor cells (HPC) of MS patients is pre-conditioned to re-develop the proinflammatory phenotype. The objective of this article is to compare the whole genome gene and microRNA expression signature in CD34+ HPC of MS patients and healthy donors (HD). CD34+ HPC were isolated from peripheral blood of eight MS patients and five HD and analyzed by whole genome gene expression and microRNA expression microarray. Among the differentially expressed genes (DEGs) only TNNT1 reached statistical significance (logFC=3.1, p<0.01). The microRNA expression was not significantly different between MS patients and HD. We did not find significant alterations of gene expression or microRNA profiles in CD34+ HPCs of MS patients. Our results support the use of aHSCT for treatment of MS.