ArticleActa anaesthesiologica Scandinavica2011
Isoflurane decreases death of human embryonic stem cell-derived, transcriptional marker Nkx2.5(+) cardiac progenitor cells.
Article in Acta anaesthesiologica Scandinavica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Isoflurane decreases proliferation and differentiation, but none of the effects persist in human embryonic stem cell-derived neural progenitor cells.Journal of anesthesia · 2017Article
- The involvement of protein kinase C-ε in isoflurane induced preconditioning of human embryonic stem cell--derived Nkx2.5(+) cardiac progenitor cells.BMC anesthesiology · 2016Article
- Preconditioning stem cells for in vivo delivery.BioResearch open access · 2014Review
- Cell based therapies for ischemic stroke: from basic science to bedside.Progress in neurobiology · 2014Review
- Engineering the human pluripotent stem cell microenvironment to direct cell fate.Biotechnology advances · 2013Review
- Concise review: maturation phases of human pluripotent stem cell-derived cardiomyocytes.Stem cells (Dayton, Ohio) · 2013Review
- Dual effects of isoflurane on proliferation, differentiation, and survival in human neuroprogenitor cells.Anesthesiology · 2013Article
- Preconditioning strategy in stem cell transplantation therapy.Translational stroke research · 2013Review
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundCardiac progenitor cells (CPCs) derived from human embryonic stem cells (hESCs) can multiply and generate cardiomyocytes, offering their tremendous potential for cardiac regenerative therapy. However, poor survival under stressful conditions is a major hurdle in the regeneration. We investigated whether isoflurane-induced preconditioning can increase hESC-derived CPC survival under oxidative stress.
methodsUndifferentiated hESCs were cultured in suspension with 20% FBS (fetal bovine serum) and 20 ng/ml of BMP-4 (bone morphogenetic protein-4) to form embryoid bodies and grown onto Matrigel-coated plates for 2-3 weeks. To characterise the differentiated CPCs, immunostaining for Nkx2.5 (nonspecific transcriptional marker) and Isl-1 was performed. hESC-derived CPCs were exposed to oxidative stress induced by H(2) O(2) and FeSO(4) . For anaesthetic preconditioning, CPCs were exposed to isoflurane (0.25, 0.5, 1.0 mM). CPC survival was determined by trypan blue exclusion. A mitoK(ATP) channels inhibitor, 5-hydroxydecanoic acid (200 μM) and an opener, diazoxide (100 μM), were used to investigate the involvement of mitoK(ATP) channels.
resultshESC-derived CPCs stained with Nkx2.5 were 95 ± 3% of total cell number. Isoflurane (0.5 and 1.0 mM)-preconditioned CPCs showed a significantly lower death rate compared with control (0.5 mM: 30.6 ± 10.7% and 1.0 mM: 28.5 ± 6.2% vs. control: 43.2 ± 9.9%). Inhibition of mitoK(ATP) channels with 5-HD completely abolished the protective effects of isoflurane. Diazoxide significantly decreased CPC death (29.5 ± 12.4%). However, when diazoxide was applied to CPC preconditioned with isoflurane, CPC death did not decrease further (28.7 ± 10.9%).
conclusionIsoflurane increased hESC-derived Nkx2.5(+) CPC survival under oxidative stress, and mitoK(ATP) channels may be involved in the protective effect.
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