ArticleBMC biotechnology2008
Pharmaceutical induction of ApoE secretion by multipotent mesenchymal stromal cells (MSCs).
Article in BMC biotechnology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
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6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundApolipoprotein E (ApoE) is a molecular scavenger in the blood and brain. Aberrant function of the molecule causes formation of protein and lipid deposits or "plaques" that characterize Alzheimer's disease (AD) and atherosclerosis. There are three human isoforms of ApoE designated epsilon2, epsilon3, and epsilon4. Each isoform differentially affects the structure and function of the protein and thus the development of disease. Homozygosity for ApoE epsilon4 is associated with atherosclerosis and Alzheimer's disease whereas ApoE epsilon2 and epsilon3 tend to be protective. Furthermore, the epsilon2 form may cause forms of hyperlipoproteinemia. Therefore, introduction of ApoE epsilon3 may be beneficial to patients that are susceptible to or suffering from these diseases. Mesenchymal stem cells or multipotent mesenchymal stromal cells (MSCs) are adult progenitor cells found in numerous tissues. They are easily expanded in culture and engraft into host tissues when administered appropriately. Furthermore, MSCs are immunosuppressive and have been reported to engraft as allogeneic transplants. In our previous study, mouse MSCs (mMSCs) were implanted into the brains of ApoE null mice, resulting in production of small amounts of ApoE in the brain and attenuation of cognitive deficits. Therefore human MSCs (hMSCs) are a promising vector for the administration of ApoE epsilon3 in humans.
resultsUnlike mMSCs, hMSCs were found not to express ApoE in culture; therefore a molecular screen was performed for compounds that induce expression. PPARgamma agonists, neural stem cell conditioned medium, osteo-inductive media, dexamethasone, and adipo-inductive media (AIM) were tested. Of the conditions tested, only AIM or dexamethasone induced sustained secretion of ApoE in MSCs and the duration of secretion was only limited by the length of time MSCs could be sustained in culture. Upon withdrawal of the inductive stimuli, the ApoE secretion persisted for a further 14 days.
conclusionThe data demonstrated that pre-treatment and perhaps co-administration of MSCs homozygous for ApoE epsilon3 and dexamethasone may represent a novel therapy for severe instances of AD, atherosclerosis and other ApoE-related diseases.
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