Protein kinase A inhibitor, H89, enhances survival and clonogenicity of dissociated human embryonic stem cells through Rho-associated coiled-coil containing protein kinase (ROCK) inhibition

Zhang, Liang; Xu, Yanqing; Xu, Jiandong; Wei, Yuping; Xu, Xia

doi:10.1093/humrep/dew011

Cited by 14 publications

(7 citation statements)

References 38 publications

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“…These results indicated that H89 depresses PKA activation and promotes hESC survival after cryopreservation through ROCK inhibition. H89 also elevates dissociated hESC survival through ROCK inhibition as reported in our previous study . Therefore, we deduce that the increased survival of hESCs by H89 addition in the different stages of cryopreservation, including before dissociation, during freezing and following thawing (Fig.…”

Section: Discussionsupporting

confidence: 82%

Protein kinase A inhibitor, H89, significantly enhances survival rate of dissociated human embryonic stem cells following cryopreservation

Zhang

et al. 2016

Cell Proliferation

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Section: Discussionsupporting

confidence: 82%

Protein kinase A inhibitor, H89, significantly enhances survival rate of dissociated human embryonic stem cells following cryopreservation

Zhang

et al. 2016

Cell Proliferation

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“…Meanwhile, L. Zhang et al . found that PKA selective inhibitor H89 up-regulated both p-PKA and total PKA expression in a time dependent manner 40 . In accordance with our results, these studies confirm the long term treatment of functional PKG or PKA inhibitors not only regulates the function, but also the expression of the target proteins.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of PDE2 reverses beta amyloid induced memory impairment through regulation of PKA/PKG-dependent neuro-inflammatory and apoptotic pathways

Wang

Xiaokaiti

Wang

et al. 2017

Sci Rep

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Beta amyloid peptides (Aβ) are known risk factors involved in cognitive impairment, neuroinflammatory and apoptotic processes in Alzheimer’s disease (AD). Phosphodiesterase 2 (PDE2) inhibitors increase the intracellular cAMP and/or cGMP activities, which may ameliorate cognitive deficits associated with AD. However, it remains unclear whether PDE2 mediated neuroapoptotic and neuroinflammatory events, as well as cognitive performance in AD are related to cAMP/cGMP-dependent pathways. The present study investigated how the selective PDE2 inhibitor BAY60-7550 (BAY) affected Aβ-induced learning and memory impairment in two classic rodent models. IL-22 and IL-17, Bax and Bcl-2, PKA/PKG and the brain derived neurotropic factor (BDNF) levels in hippocampus and cortex were detected with immunoblotting assay. The results showed that BAY reversed Aβ-induced cognitive impairment as shown in the water maze test and step-down test. Moreover, BAY treatment reversed the Aβ-induced changes in IL-22 and IL-17 and the ratio of Bax/Bcl-2. Changes in cAMP/cGMP levels, PKA/PKG and BDNF expression were also prevented by BAY. These effects of BAY on memory performance and related neurochemical changes were partially blocked by the PKG inhibitor KT 5823. These findings indicated that the protective effects of BAY against Aβ-induced memory deficits might involve the regulation of neuroinflammation and neuronal apoptotic events.

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“…H89 is a multi-target molecule that regulates lots of targets and pathways [45–47]. Thus, on one hand, these pathways might indirectly modulate the Epac1 activities.…”

Section: Discussionmentioning

confidence: 99%

A classical PKA inhibitor increases the oncolytic effect of M1 virus via activation of exchange protein directly activated by cAMP 1

Liang

Lin

et al. 2016

Oncotarget

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Oncolytic virotherapy is an emerging and promising treatment modality that uses replicating viruses as selective antitumor agents. Here, we report that a classical protein kinase A (PKA) inhibitor, H89, synergizes with oncolytic virus M1 in various cancer cells through activation of Epac1 (exchange protein directly activated by cAMP 1). H89 substantially increases viral replication in refractory cancer cells, leading to unresolvable Endoplasmic Reticulum stress, and cell apoptosis. Microarray analysis indicates that H89 blunts antiviral response in refractory cancer cells through retarding the nuclear translocation of NF-κB. Importantly, in vivo studies show significant antitumor effects during M1/H89 combination treatment. Overall, this study reveals a previously unappreciated role for H89 and demonstrates that activation of the Epac1 activity can improve the responsiveness of biotherapeutic agents for cancer.

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Protein kinase A inhibitor, H89, enhances survival and clonogenicity of dissociated human embryonic stem cells through Rho-associated coiled-coil containing protein kinase (ROCK) inhibition

Abstract: Nil.

Cited by 14 publications

References 38 publications

Protein kinase A inhibitor, H89, significantly enhances survival rate of dissociated human embryonic stem cells following cryopreservation

Protein kinase A inhibitor, H89, significantly enhances survival rate of dissociated human embryonic stem cells following cryopreservation

Inhibition of PDE2 reverses beta amyloid induced memory impairment through regulation of PKA/PKG-dependent neuro-inflammatory and apoptotic pathways

A classical PKA inhibitor increases the oncolytic effect of M1 virus via activation of exchange protein directly activated by cAMP 1

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