Effects of the protein phosphatase inhibitors okadaic acid and calyculin A on metabolically inhibited and ischaemic isolated myocytes
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Cited by (46)
Connexin channel and its role in diabetic retinopathy
2017, Progress in Retinal and Eye ResearchCitation Excerpt :Work by Kondo et al. demonstrated removal of extracellular [Ca2+] and metabolic inhibition can activate non-selective electrical current, which may impact ionic fluxes, and promote arrhythmias and myocardial infarction (Kondo et al., 2000). The activity of phosphatases and protein kinases is elevated whereas Cx43 is dephosphorylated during myocardial ischemia (Armstrong and Ganote, 1992; Beardslee et al., 2000). In other studies, mitogen-activated protein kinases (MAPK), PKC and PTK signaling pathways are reported to be involved in cardiac protection during ischemia (Weinbrenner et al., 1998).
Zinc plays a critical role in the cardioprotective effect of postconditioning by enhancing the activation of the RISK pathway in rat hearts
2014, Journal of Molecular and Cellular CardiologyCitation Excerpt :In support, PP2A inhibition with fostriecin has been demonstrated to protect rabbit hearts from ischemia/reperfusion injury [38]. Similarly, inhibition of protein phosphatases with okadaic acid or calyculin A could protect cardiomyocytes from ischemic injury [39]. However, since these chemicals may also act on other subtypes of Ser/Thr protein phosphatases, more studies are required to determine if other protein phosphatases are also involved in the activation of the RISK pathway by ischemic postconditioning.
Biological role of connexin intercellular channels and hemichannels
2012, Archives of Biochemistry and BiophysicsCitation Excerpt :Kondo et al. [59] show electrophysiologically that removal of extracellular [Ca2+] and metabolic inhibition allows activation of non-selective current which may have a role in alteration of ionic fluxes thereby promoting arrhythmias and myocardial infarction. During myocardial ischemia, Cx43 is dephosphorylated and activity of several protein kinases and phosphatases gets affected [60–62]. The initiation of ischemia which accounts for the first few minutes does not affect the partially phosphorylated status of the physiological sarcolemmal Cx43 [63].
Enhanced cell volume regulation: A key protective mechanism of ischemic preconditioning in rabbit ventricular myocytes
2003, Journal of Molecular and Cellular CardiologyOkadaic acid, an inhibitor of protein phosphatase, exerts a protective effect on ischemia-reperfusion injury in rat kidneys
2002, Transplantation Proceedings