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Abstract
Extracellular vesicles (EVs) play a significant role in cell–cell communication in numerous physiological processes and pathological conditions, and offer promise as novel biomarkers and therapeutic agents for genetic diseases. Many recent studies have described different molecular mechanisms that contribute to EV biogenesis and release from cells. However, little is known about how external stimuli such as cell culture conditions can affect the quantity and content of EVs. While N2a neuroblastoma cells cultured in serum-free (OptiMEM) conditions did not result in EVs with significant biophysical or size differences compared with cells cultured in serum-containing (pre-spun) conditions, the quantity of isolated EVs was greatly increased. Moreover, the expression levels of certain vesicular proteins (e.g. small GTPases, G-protein complexes, mRNA processing proteins and splicing factors), some of which were previously reported to be involved in EV biogenesis, were found to be differentially expressed in EVs under different culture conditions. These data, therefore, contribute to the understanding of how extracellular factors and intracellular molecular pathways affect the composition and release of EVs.
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Acknowledgements
JHL, IM and the project are supported by an EU IMI funding programme (COMPACT). YL is supported by Agency for Science, Technology and Research (A*STAR), Singapore. IM was supported by a Postdoctoral MOBILITAS Fellowship of Estonian Science Foundation and by the Estonian Research Council Grant PUT618. PV is supported by a Rubicon Fellowship from the Netherlands Organisation for Scientific Research (NWO). JN and OW are both recipients of Karolinska Institutet MD/PhD grants. S.ELA is supported by the Swedish Medical Research Council (VR-Med), Swedish Society of Medical Research (SSMF) and EuroNanoMedII. HJ and JL are supported by the Swedish Research Council (VR-NT) and Swedish Cancer Society.
Notes
To access the supplementary material to this article, please see Supplementary files under ‘Article Tools’.