I know the discussion (http://hardcorephysiologyfun.blogspot.com/2009/01/myogenic-satellite-cells-mitochondrial.html) about the transfer of mutant mtDNA into myocytes, in reference to this article [Taivassalo and Haller, 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15576055)], might sound far-fetched, and I suppose it's conceivable that the satellite cells differentiate into myocytes. But the article does contain a discussion about the apparent transfer, from the satellite cells to the myocytes, of nuclei and mtDNA and other intracellular constituents. The authors cite references 42, 43, 48, and 50 as evidence, and one of their citations is a book on satellite cells. This is another article that discusses the capacity of satellite cells to restore mtDNA in damaged or myocytes [Smith et al., 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15576056)].
That concept of the uptake of DNA has been shown in other cell types and is thought to occur in melanosomes, I think, which are pigment-containing "granules" that are released by melanocytes but that can also contain intracellular proteins, such as proliferating cell nuclear antigen (PCNA) [Iyengar, 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9585249)]. It's almost similar to or reminiscent of some axonal transport mechanisms that have been proposed, too. I know this type of thing may be controversial, but I'm just thinking out loud and thinking about the full range of mechanisms that have been discussed in these areas. And I know that perineuronal satellite cells are phenotypically distinct from myogenic satellite cells, but is a process going to be totally unique to myogenic satellite cells? There are many articles saying they're pluripotent, and presumably that would imply that some of their functions are at least somewhat generalizable to other, pluripotent or multipotent cells in different parts of the brain. Even if one rejects the mechanism of mtDNA transfer, there is some mechanism to explain the association between satellite cell proliferation and the restoration of wild-type mtDNA in myocytes.
Another reason I mention purines in the context of reduced folates and neuronal progenitor cells is that the de novo purine biosynthetic capacities of mitotic cells tend to be much higher than the capacities of postmitotic or nonmitotic cells, such as postmitotic neurons (which have staggeringly low capacities for purine biosynthesis). Here's an interesting article showing that neuronal progenitor cells derived from the subventricular zone, in the brain, release purines into the extracellular space in "bursts" [Lin et al., 2007: (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1924912) (http://www.ncbi.nlm.nih.gov/pubmed/17188262)]. This would suggest that, to the extent that reduced folates, such as L-methylfolate or L-leucovorin, can increase neuronal progenitor cell proliferation [here's one article that shows that folate deficiency reduces the numbers of neuronal progenitor cells in the hippocampus, and the authors cite some other articles showing suppression of neurogenesis in response to folate depletion: Kronenberg et al., 2008: (http://www.jneurosci.org/cgi/content/full/28/28/7219) (http://www.ncbi.nlm.nih.gov/pubmed/18614692)], the cells, as shown by Lin et al. (2007), could release purines before they die off. Even though many progenitor cells do die off in the brain and do not differentiate into mature neurons, their release of purines into the interstitual fluid in the brain could reasonably be expected to exert trophic effects.
The articles on the effects of oral purines, such as this one [Kichenin et al., 2000: (http://jpet.aspetjournals.org/cgi/content/full/294/1/126) (http://www.ncbi.nlm.nih.gov/pubmed/10871303)], show the way in which purines can be transported en masse into cells and produce only transient, localized [as in the portal blood, shown by Kichenin et al. (2000)] increases in the concentrations of serum adenosine or other purines. It's only when the cells are extracted, as Kichenin et al. (2000) discussed, that the effects become apparent. The extracellular adenosine, derived from red blood cells (RBC) in rabbits given intrajejunal infusions of adenosine 5'-triphosphate, was much larger than the RBC-derived adenosine from control rabbits, and the intracellular ATP levels were also substantially increased in the RBC from the ATP-treated rabbits [Kichenin et al., 2000]. By the same token, the contribution of neural progenitor cell-derived purines to intracellular purine pools in neurons or astrocytes may be highly localized. The purines (and probably pyrimidines also) released by neural progenitor cells could then support mtDNA replication in neurons or astrocytes that have diminished pools of purines and pyrimidines, such as can result from mtDNA depletion and the mitochondrial dysfunction that tends to result from mtDNA depletion (http://hardcorephysiologyfun.blogspot.com/2008/12/heteroplasmy-mtdna-copy-number-uridine.html).
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