Format

Send to

Choose Destination
Sci Rep. 2018 Jan 29;8(1):1756. doi: 10.1038/s41598-018-19703-5.

SPK1-transfected UCMSC has better therapeutic activity than UCMSC in the treatment of experimental autoimmune encephalomyelitis model of Multiple sclerosis.

Author information

1
Department of Neurology, the Second Affiliated Hospital of Zhengzhou University, No. 32 Nanyang Road, Zhengzhou, 450014, China.
2
Department of Neurology, the 148th Hospital of Chinese PLA, No. 20 North Road Zhoucun District, Zibo, 255300, China.
3
Electroencephalogram Room of Sanbo Brain Hospital, Capital Medical University, No. 50 Xiangshanyikesong Haidian District, Beijing, 100093, China.
4
Department of Experimental Hematology, Beijing Institute of Radiation Medicine, Beijing, 100850, China. duanhf0720@163.com.
5
Department of Medical Oncology, Chinese PLA General Hospital, Beijing, 100853, China. jinfenglidoc@163.com.

Abstract

Multiple Sclerosis (MS), is a chronic inflammatory autoimmune disorder of the central nervous system that leads to chronic demyelination with axonal damage and neuronal loss. Mesenchymal stem cells (MSCs) represent a promising therapeutic approach for MS. In the current study, we investigated the effects of MSCs derived from the human umbilical cord (UCMSC) transfected by sphingosine kinase 1 (SPK1) gene. All the results showed that transplantation of UCMSCs gene modified by SPK1 (UCMSC-SPK1) dramatically reduce the severity of neurological deficits of the experimental autoimmune encephalomyelitis (EAE) mice, paralleling by reductions in demyelination, axonal loss, and astrogliosis. UCMSC-SPK1 transplantation also could inhibit the development of natural killer (NK) responses in the spleen of EAE mice, and increase the ratio of CD4+ CD25+ FoxP3+ (Treg) T cells. Furthermore, we described that a shift in the cytokine response from Th1/Th17 to Th2 was an underlying mechanism that suppressed CNS autoimmunity. UCMSCs transfected by SPK1 gene potentially offer a novel mode for the treatment of MS, and the specific mechanism of SPK1 in treating MS/EAE.

PMID:
29379030
PMCID:
PMC5788935
DOI:
10.1038/s41598-018-19703-5
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center