An Attempt to Compensate for Deficiencies in Stem Cells Derived from Heart Failure Patients

One of the ongoing themes in stem cell research is that cells and environments in old people do not function correctly, this interferes with most potential treatments in numerous ways, and thus scientists are in search of fixes and workarounds. Most potential applications of regenerative therapies involve the treatment of age-related diseases, and so the industry must address these issues in order to succeed. It is good for all of us that this incentive exists, as it spurs progress in an important area of research. The paper referenced below is a modest example of one approach in this field, in which researchers catalog some of the differences between the stem cells of healthy individuals and heart failure patients, noting that these cause issues when trying to expand a cell sample into a large enough number of cells for a transplant treatment:

Chronic heart failure (HF) is one of the most common causes of death worldwide, and the only radical treatment for severe chronic HF remains to be heart transplantation. It is necessary to search for new therapeutic approaches to restore the structure and function of cardiac muscle. In the past two decades cell therapy has been considered as the prospective therapeutic approach to the treatment of cardiovascular diseases including HF. The cells intended for cell therapy must have certain characteristics: they should be relatively easy available, safe, and demonstrate efficiency in stimulation of reparation of cardiac muscle. Different cell types were tested in regeneration protocols and by now multipotent mesenchymal stromal cells from bone marrow (BM-MMSC) remain to be the most attractive, and one of the best characterized substrates for clinical applications: these cells could be rapidly and efficiently expanded in vitro and this type of cells is known to be immunologically privileged.

Many researchers still believe that the ideal substrate for cell therapy are autologous cells. However, it was demonstrated in several animal-based studies that donor-specific factors could attenuate stem cell functions and reduce regenerative potential. Influence of donor's age and gender on the properties of BM-MMSC has been studied actively in recent years in many laboratories, but the studies of impact of chronic cardiovascular disorders, including HF, on multipotent progenitor cells are limited.

In present work we have found that a number of properties were altered in BM-MMSC derived from HF patients compared to healthy donor-derived BM-MMSC. In particular, in HF-derived BM-MMSC a decrease in proliferative activity during in vitro expansion was detected, accompanied by upregulation of signaling pathways that control both tissue regeneration and fibrosis. We have demonstrated that decrease in efficiency of expansion could be markedly improved by culturing of BM-MMSC under moderate hypoxic conditions and substantial decrease in cell seeding density. Further experiments are necessary to learn how to manipulate the culturing conditions in order to predict and, most importantly, control the balance between proliferation rate, replicative senescence, regenerative potential, pro-fibrotic and anti-fibrotic properties of cellular sample intended for experimental or therapeutic protocols.



It should come as a surprise to absolutely no one that cells derived from an aged patient are not as good as cells derived from a younger one.

The next obvious step would be to fix the cells...

Posted by: Slicer at January 16th, 2015 1:15 PM

Also, Reason, your HTML is broken; an unclosed quote in the first Heart Failure link chops a big chunk out of the quote.

Posted by: Slicer at January 17th, 2015 2:56 PM

@Slicer: Fixed.

Posted by: Reason at January 17th, 2015 2:59 PM

And working now.

Posted by: Slicer at January 17th, 2015 3:00 PM

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