European Journal of Pharmacology: Molecular Pharmacology
Regular paperDual effects of protein kinase-C on receptor-stimulated cAMP accumulation in a human T-cell leukemia line
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Cardiovascular adenosine receptors: Expression, actions and interactions
2013, Pharmacology and TherapeuticsCitation Excerpt :However, protection via PKC activation can be negated by A2BR antagonism, and PKC and PreCon both lower the threshold for AR-dependent kinase phosphorylation (Philipp et al., 2006; Kuno et al., 2007). Modulation of A2BR sensitivity is consistent with PKC-dependent sensitization of A2R-mediated responses in other cells (Nordstedt et al., 1989; Nash et al., 1997), and effects of A2BR deletion confirm a role for this receptor in conditioning responses (Eckle et al., 2007). This process may contribute to AR cross-talk in cardioprotection: since A1Rs activate PKC, and are activated during ischemia and PreCon (Thornton et al., 1992; Toombs et al., 1992; Zhao et al., 1994; Headrick, 1996; Louttit et al., 1999; Peart & Headrick, 2000), A1Rs may promote A2BR-mediated protection, consistent with A2A/A2BR dependence of A1R protection (Lasley et al., 2007; Urmaliya et al., 2010; Zhan et al., 2011).
Adenosine and its receptors in the heart: Regulation, retaliation and adaptation
2011, Biochimica et Biophysica Acta - BiomembranesCitation Excerpt :This is underpinned primarily by data in rabbit hearts, though A2BAR dependence of conditioning responses is supported by knockout studies in mice [14]. Modulation of A2BAR sensitivity is also consistent with PKC-dependent sensitization of A2AR responses in other cell types [185,186]. As discussed below, this mechanism may contribute to both PreC and postconditioning (PostC).
Protein kinase C protects preconditioned rabbit hearts by increasing sensitivity of adenosine A<inf>2b</inf>-dependent signaling during early reperfusion
2007, Journal of Molecular and Cellular CardiologyCitation Excerpt :We are not the first to see this effect. In Jurkat cells PKC activation greatly enhances the cAMP response from NECA [17]. A similar effect was seen in retinal cells [18].
Evidence against adenosine analogues being agonists at the growth hormone secretagogue receptor
2005, Biochemical PharmacologyCitation Excerpt :It could, however, be that there are major interactions between the signaling pathways. Previous results have shown that signaling via A2B receptors can be very strongly affected by signals via other receptors [20]. We first studied if there was an additive or synergistic effect in calcium response when the co-transfected cells were stimulated with both NECA and hGhrelin, but we could not find any synergistic effect (Fig. 1D).