Pinacidil enhances survival of cryopreserved human embryonic stem cells

Barbaric, Ivana; Jones, Mark; Buchner, Kristina; Baker, Duncan; Andrews, Peter W.; Moore, H. D. M.

doi:10.1016/j.cryobiol.2011.10.002

Cited by 23 publications

(17 citation statements)

References 27 publications

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“…Furthermore, pinacidil pre-treatment was able to exert significant protective effects following hemorrhagic shock, mainly by the activation of protein kinase C (PKC)α and PKCε via adenosine receptor A1, which restored vascular reactivity and calcium sensitivity and influenced the success of hemorrhagic shock therapy (4). Pinacidil was also demonstrated to enhance the survival of cryopreserved human embryonic stem cells (hESCs) (5). Following plating of thawed hESCs, pinacidil significantly enhanced cell attachment capacity.…”

Section: Introductionmentioning

confidence: 97%

Pinacidil protects osteoblastic cells against antimycin A-induced oxidative damage

Choi

Jung

Suh

2014

Molecular Medicine Reports

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Section: Introductionmentioning

confidence: 97%

Pinacidil protects osteoblastic cells against antimycin A-induced oxidative damage

Choi

Jung

Suh

2014

Molecular Medicine Reports

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“…Another study confirmed that Y-27632, HA1004, HA1077, H-89 (all kinase inhibitors) and pinacidil promote hESC viability, (Barbaric et al, 2010b), overall suggesting that the activities of multiple kinases, such as PRK2, ROCK, MAP kinase interacting serine/ threonine kinase 1 (MNK1) and ribosomal protein S6 kinases (RSK1 and MSK1), may all be necessary for the survival of hESCs. A recent report has additionally shown that pinacidil and Y-27632 aid cryopreservation of hESCs (Barbaric et al, 2011). Finally, Y-27632 has also proven to be important during hESC differentiation.…”

Section: Embryonic Stem Cell Survivalmentioning

confidence: 99%

Potential for pharmacological manipulation of human embryonic stem cells

Atkinson

Lako

Armstrong

2013

British J Pharmacology

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The therapeutic potential of human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) is vast, allowing disease modelling, drug discovery and testing and perhaps most importantly regenerative therapies. However, problems abound; techniques for cultivating self‐renewing hESCs tend to give a heterogeneous population of self‐renewing and partially differentiated cells and general include animal‐derived products that can be cost‐prohibitive for large‐scale production, and effective lineage‐specific differentiation protocols also still remain relatively undefined and are inefficient at producing large amounts of cells for therapeutic use. Furthermore, the mechanisms and signalling pathways that mediate pluripotency and differentiation are still to be fully appreciated. However, over the recent years, the development/discovery of a range of effective small molecule inhibitors/activators has had a huge impact in hESC biology. Large‐scale screening techniques, coupled with greater knowledge of the pathways involved, have generated pharmacological agents that can boost hESC pluripotency/self‐renewal and survival and has greatly increased the efficiency of various differentiation protocols, while also aiding the delineation of several important signalling pathways. Within this review, we hope to describe the current uses of small molecule inhibitors/activators in hESC biology and their potential uses in the future.LINKED ARTICLES This article is part of a themed section on Regenerative Medicine and Pharmacology: A Look to the Future. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2013.169.issue‐2

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“…These cells were derived from the inner cell mass (ICM) of grade III poor quality blastocysts that were not suitable for in vitro fertility treatment. Both the lines as claimed by JNCASR are pluripotent and have been extensively characterized and cultured continuously for over 250 passages [28][29][30][31][32][33][34][35].…”

Section: Expansion Of Human Embryonic Stem Cells (Bjnhem19 and Bjnhem20)mentioning

confidence: 99%

“…The cellular response to heat shock includes the transcriptional up-regulation of genes encoding heat shock proteins (HSPs) as part of the cell's internal repair mechanism [30]. They are also called stress-proteins [31] and respond to heat, cold and oxygen deprivation by activating several cascade pathways [32][33][34][35]. Mixed phenotype in SAGM with transient hears shock (BJnhem20).…”

Section: Additional Stimuli For Inductionmentioning

confidence: 99%