Archives for May 21, 2012

Multiple Sclerosis Treatment Success Using Mesenchymal Stem Cell-Secreted Factors in Animal Model

Stem cell researchers at Case Western Reserve have reported in Nature Magazine that the functional deficits caused by multiple sclerosis can be reduced by administering mesenchymal stem cell secreted factors.

While previous studies have shown promising results using mesenchymal stem cells, this is the first time that such results have been reported without using the stem cells themselves.

The Stem Cell Institute’s Founder, Neil Riordan PhD, originally cited the potential therapeutic role of mesenchymal stem cell trophic factors in the 2010 Cellular Immunology publication: Mesenchymal Stem Cells as Anti-inflammatories: Implications for Treatment of Duchenne Muscular Dystrophy

In addition to reducing functional deficits, the development of new myelinating oligodendrocytes and neurons, release of inflammatory cytokines, and suppression of immune cells influx were also observed in the Case Western study.

Details can be found here:

Hepatocyte growth factor mediates mesenchymal stem cell–induced recovery in multiple sclerosis models

Lianhua Bai, Donald P Lennon, Arnold I Caplan, Anne DeChant, Jordan Hecker, Janet Kranso, Anita Zaremba Robert H Miller

Nature Neuroscience (2012) doi:10.1038/nn.3109
Received 18 January 2012 Accepted 17 April 2012 Published online 20 May 2012


Mesenchymal stem cells (MSCs) have emerged as a potential therapy for a range of neural insults. In animal models of multiple sclerosis, an autoimmune disease that targets oligodendrocytes and myelin, treatment with human MSCs results in functional improvement that reflects both modulation of the immune response and myelin repair. Here we demonstrate that conditioned medium from human MSCs (MSC-CM) reduces functional deficits in mouse MOG35–55-induced experimental autoimmune encephalomyelitis (EAE) and promotes the development of oligodendrocytes and neurons. Functional assays identified hepatocyte growth factor (HGF) and its primary receptor cMet as critical in MSC-stimulated recovery in EAE, neural cell development and remyelination. Active MSC-CM contained HGF, and exogenously supplied HGF promoted recovery in EAE, whereas cMet and antibodies to HGF blocked the functional recovery mediated by HGF and MSC-CM. Systemic treatment with HGF markedly accelerated remyelination in lysolecithin-induced rat dorsal spinal cord lesions and in slice cultures. Together these data strongly implicate HGF in mediating MSC-stimulated functional recovery in animal models of multiple sclerosis.