Subtype-specific neuronal differentiation of PC12 cells transfected with α2-adrenergic receptors
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Sustained GRK2-dependent CREB activation is essential for α<inf>2</inf>-adrenergic receptor-induced PC12 neuronal differentiation
2020, Cellular SignallingCitation Excerpt :# G9500; Promega US, Madison, WI, USA). For differentiation experiments, cells were plated (50,000 cells/ml) on collagen-coated culture dishes and cultured in DMEM supplemented with 1% horse serum and 10 mM MgCl2 (differentiation medium), as described [9]. For morphological experiments, the percentage of cells showing neurite outgrowth was determined using phase-contrast microscopy.
Pharmacological, but not genetic, alteration of neural Epo modifies the CO<inf>2</inf>/H<sup>+</sup> central chemosensitivity in postnatal mice
2017, Respiratory Physiology and NeurobiologyCitation Excerpt :However, apart from being implicated in the molecular pathway activated by Epo (Caravagna and Soliz, 2015), ERK/Akt are also molecules involved in major processes accomplishing a wide variety of neural tasks, including glucose metabolism (Engelman et al., 2006), cellular apoptosis and survival (Teng et al., 2014), differentiation (Chan et al., 2013), neural proliferation and migration (Dey et al., 2005), neuroprotection (Zhang et al., 2015), neurodegeneration (Fang et al., 2015), and synaptic signalling (Yoshii and Constantine-Paton, 2014). Moreover, ERK/Akt in brain tissue participates in the modulation of dopaminergic (Beaulieu et al., 2006), muscarinic (Rosenblum et al., 2000), adrenergic (Taraviras et al., 2002), serotonergic (Cowen, 2007), GABAergic (Balasubramanian et al., 2004) and adenosinergic (Wiese et al., 2007) neurotransmission. As such, our results are currently limited to explain whether apart from the Epo molecular pathway, ERK/Akt modulates the hypercapnic fictive breathing by affecting other mechanisms.
GPCRs of adrenal chromaffin cells & catecholamines: The plot thickens
2016, International Journal of Biochemistry and Cell BiologyCitation Excerpt :The α2ARs are inhibitory autoreceptors that inhibit further release of CA's in adrenergic nerves in the central sympathetic nervous system (SNS), and in the adrenal medulla (Fig. 1). The predominant inhibitory role of α2ARs in the adrenal gland becomes clear when considering that PC12, a rat pheochromocytoma (chromaffin) cell line does not express these receptors and secretes abnormal catecholamine quantities (Taraviras et al., 2002). However, the mouse and rat adrenal glands, as well as the human adrenal gland (Berkowitz et al., 1994; Lymperopoulos et al., 2007a), normally express various α2AR subtypes endogenously, mainly α2A- and α2CARs (in the murine adrenal gland) (Brede et al., 2003).