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- W1650248640 startingPage "12" @default.
- W1650248640 abstract "Astroglial beta-adrenergic receptors (beta-ARs) are functionally linked to regulate cellular morphology. In primary cultures, the beta-AR agonist isoproterenol (ISP) can transform flat polygonal astrocytes into process-bearing, mature stellate cells by 48 h, an effect that can be blocked by the beta-AR antagonist, propranolol. ISP induced immediate activation of protein kinase A (PKA) which persisted up to 2 h, with no visible change in cell morphology. However, activation of PKA was sufficient to drive the process of transformation to completion, suggesting the involvement of downstream regulators of PKA. In addition to PKA inhibitors, the mitogen-activated protein kinase (MAPK) kinase inhibitor PD098059 also blocked ISP-induced morphological transformation. ISP treatment resulted in a biphasic response of cellular phosphorylated MAPK (phosphorylated extracellular signal-regulated kinase; p-ERK) level: an initial decline in p-ERK level followed by a sustained induction at 12-24 h, both of which were blocked by PKA inhibitor. The induction in pERK level coincided with initiation of morphological differentiation of the astrocytes and nuclear translocation of p-ERK. A long-lasting activation of p-ERK activity by ISP, at a later stage, appears to be critical for the transformation of astrocytes." @default.
- W1650248640 created "2016-06-24" @default.
- W1650248640 creator A5049082330 @default.
- W1650248640 creator A5082345875 @default.
- W1650248640 date "2003-11-28" @default.
- W1650248640 modified "2023-10-17" @default.
- W1650248640 title "Delayed but sustained induction of mitogen-activated protein kinase activity is associated with β-adrenergic receptor-mediated morphological differentiation of astrocytes" @default.
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