Cord Blood Differentiation to Muscle

u did see that the chinese report of a 12 year old Ducenne patient treated with 24 × 10(8) cord blood mononuclear cells and had improvement in locomotion, as well as decreased creatinine kinase and expression of dystrophin.

Zhang C, Feng HY, Huang SL, Fang JP, Xiao LL, Yao XL, Chen C, Ye X, Zeng Y, Lu XL, Wen JM, Zhang WX, Li Z, Feng SW, Xu HG, Huang K, Zhou DH, Chen W, Xie YM, Xi J, Zhang M, Li Y, Liu Y. [Therapy of Duchenne muscular dystrophy with umbilical cord blood stem cell transplantation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2005 Aug;22(4):399-405.

fusion, no transdifferentiation,
very rare events and no effect
thanks Paul for link

I never understood this whole fusion thing. When a stem cell "fuses" does the cell that comes out still function? Or is it some kind of messed up cell?

I know that monocytes and macrophages fuse to each other when they are HIV infected, maybe fusion is one of the phenotypes of stem cells and monocytes. But why on earth would cells have the ability to fuse? I mean from a physiological perspective, what advantage would that give them?

Any thoughts would be appreciated

Unfortunately, Duchenne is not as rare as stated in this item states, with 1 in every 3,500 live male births, affected.

Thats strange, I always thought it was 35,000

In any case, I noticed from your website that you keep talk about trichostatin for induction of "dedifferentiation". Did you guys see the paper by Puri's group stating that trichostatin administration is effective against Duchennes? *Functional and morphological recovery of dystrophic muscles in mice treated with deacetylase inhibitors.
Nat Med. 2006 Oct;12(10):1147-50*

So from what the literature says, Duchenne's is associated with high levels of BMP4 in the muscle of patients with this disease. The BMP4 inhibits differentiation of myocytes. This is interesting since you mentioned that BMP4 is actually involved in inducing differentiation of cancer stem cells. But in this case BMP4 is INHIBITING differentiation. This reminds me of the story of DNA methyltransferase inhibitors. On normal cells they induce expression of genes that should not be expressed. But in cancer cells they inhibit expression of oncogenic genes. For example, 5 azacytidine (Decitabine) is clinically used for a variety of indications.

Where did you see the paper describing BMP4 inhibition of muscle differentiation in DMD patients?

pubmed where else?

Neurobiol Dis. 2006 Jul;23(1):228-36. Epub 2006 May 6. Links
Gene expression profiling highlights defective myogenesis in DMD patients and a possible role for bone morphogenetic protein 4.Sterrenburg E, van der Wees CG, White SJ, Turk R, de Menezes RX, van Ommen GJ, den Dunnen JT, 't Hoen PA.
Center for Human and Clinical Genetics, Leiden University Medical Center, Einthovenweg 20, 2333 ZA Leiden, The Netherlands.

Duchenne Muscular Dystrophy (DMD) is characterized by progressive muscle weakness and wasting. Despite the sustained presence of satellite cells in their skeletal muscles, muscle regeneration in DMD patients seems inefficient and unable to compensate for the continuous muscle fiber loss. To find a molecular explanation, we compared the gene expression profiles of myoblasts from healthy individuals and DMD patients during activation and differentiation in culture. DMD cultures showed significant gene expression changes, even before dystrophin is expressed. We found a higher expression level of bone morphogenetic protein 4 (BMP4) in DMD cultures, which we demonstrate to inhibit differentiation into myotubes. In the later stages of differentiation, we observed a significant decline in expression of sarcomeric genes in the absence of dystrophin, probably contributing to sarcomeric instability. These results support the hypothesis that inefficient muscle regeneration is caused by impaired myoblast differentiation and impaired maintenance of the myotubes.

So if BMP4 induces cancer stem cell differentiation, and DMD patients have high levels of BMP4, then do these patients have less incidence of cancer?

Well this paper says there is a positive correlation between the disorder and some rare cancer. Look, these patients have some many other abnormalities besides the dystrophin gene, that I am not surprised that this is so

As the son of a toddler with Duchenne, I can verify Deb's statement that it does indeed affect 1 in 3,500 boys, not 1 in 35,000.
Even more of a reason to continue looking for treatments!
Thanks,
Lyndsey

Dear Lyndsey,

We are sorry to hear about your son. Please allow us to ask you a question. We were thinking about including a section with ongoing Stem Cell clinical trials. Do you think that would be useful? Or do you think it would be redundant with other things on the internet?

Your input is appreciated !!

StemCellPatents.com Team