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Physiology of Ca(2+) signalling in stem cells of different origins and differentiation stages

O. Forostyak, S. Forostyak, S. Kortus, E. Sykova, A. Verkhratsky, G. Dayanithi,

. 2016 ; 59 (2-3) : 57-66. [pub] 20160217

Language English Country Netherlands

Document type Journal Article, Research Support, Non-U.S. Gov't, Review

Persistent link   https://www.medvik.cz/link/bmc17014084

Stem cells (SCs) of different origins have brought hope as potential tools for the treatment of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Amyotrophic Lateral Sclerosis. Calcium signalling plays a key role in SC differentiation and proliferation, and dysregulation of Ca(2+) homeostasis may instigate pathological scenarios. Currently, the role of ion channels and receptors in SCs is not fully understood. In the recent years, we found that (i) the pre-differentiation of human embryonic SCs (hESCs) led to the activation of Ca(2+) signalling cascades and enhanced the functional activities of these cells, (ii) the Ca(2+) homeostasis and the physiological properties of hESC-derived neural precursors (NPs) changed during long term propagation in vitro, (iii) differentiation of NPs derived from human induced pluripotent SCs affects the expression of ion channels and receptors, (iv) these neuronal precursors exhibited spontaneous activity, indicating that their electrophysiological and Ca(2+) handling properties are similar to those of mature neurones, and (v) in mesenchymal SCs isolated from the adipose tissue and bone marrow of rats the expression profile of ion channels and receptors depends not only on the differentiation conditions but also on the source from which the cells were isolated, indicating that the fate and functional properties of the differentiated cells are driven by intrinsic mechanisms. Together, identification and assignment of a unique ion channel and a Ca(2+) handling footprint for each cell type would be necessary to qualify them as physiologically suitable for medical research, drug screening, and cell therapy.

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$a Forostyak, Oksana $u Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, Prague 14220, Czech Republic; Department of Neuroscience, Charles University, Second Faculty of Medicine, V Uvalu 84, 15006 Prague, Czech Republic. Electronic address: oxfor@biomed.cas.cz.
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$a Stem cells (SCs) of different origins have brought hope as potential tools for the treatment of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Amyotrophic Lateral Sclerosis. Calcium signalling plays a key role in SC differentiation and proliferation, and dysregulation of Ca(2+) homeostasis may instigate pathological scenarios. Currently, the role of ion channels and receptors in SCs is not fully understood. In the recent years, we found that (i) the pre-differentiation of human embryonic SCs (hESCs) led to the activation of Ca(2+) signalling cascades and enhanced the functional activities of these cells, (ii) the Ca(2+) homeostasis and the physiological properties of hESC-derived neural precursors (NPs) changed during long term propagation in vitro, (iii) differentiation of NPs derived from human induced pluripotent SCs affects the expression of ion channels and receptors, (iv) these neuronal precursors exhibited spontaneous activity, indicating that their electrophysiological and Ca(2+) handling properties are similar to those of mature neurones, and (v) in mesenchymal SCs isolated from the adipose tissue and bone marrow of rats the expression profile of ion channels and receptors depends not only on the differentiation conditions but also on the source from which the cells were isolated, indicating that the fate and functional properties of the differentiated cells are driven by intrinsic mechanisms. Together, identification and assignment of a unique ion channel and a Ca(2+) handling footprint for each cell type would be necessary to qualify them as physiologically suitable for medical research, drug screening, and cell therapy.
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$a Forostyak, Serhiy $u Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, Prague 14220, Czech Republic; Department of Neuroscience, Charles University, Second Faculty of Medicine, V Uvalu 84, 15006 Prague, Czech Republic.
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$a Kortus, Stepan $u Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, Prague 14220, Czech Republic; Institute of Physiology, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Institute of Biophysics and Informatics, First Medical Faculty, Charles University, Salmovska 1, 12000 Prague, Czech Republic.
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$a Sykova, Eva $u Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, Prague 14220, Czech Republic; Department of Neuroscience, Charles University, Second Faculty of Medicine, V Uvalu 84, 15006 Prague, Czech Republic.
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$a Verkhratsky, Alexei $u University of Manchester, School of Biological Sciences, D.4417 Michael Smith Building, Oxford Road, Manchester M13 9PT, UK; Achucarro Center for Neuroscience, IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain; Department of Neurosciences, University of the Basque Country UPV/EHU and CIBERNED, Leioa, Spain.
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$a Dayanithi, Govindan $u Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, Prague 14220, Czech Republic; Institut National de la Santé et de la Recherche Médicale, Unité de recherche U1198 and University of Montpellier, 34095 Montpellier, France; Ecole Pratique des Hautes Etudes-Sorbonne, Les Patios Saint-Jacques, 4-14 rue Ferrus, 75014 Paris, France. Electronic address: gdaya@univ-montp2.fr.
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