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Title: Actions of pharmacologically-distinct forms of protein kinase C in rat anterior pituitary cells
Author: MacEwan, David J.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1992
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The actions of protein kinase C (PKC) on several aspects of cellular control of Ca2+ movement were investigated in rat anterior pituitary cells. Depolarising concentrations of K+ induced influx of 45Ca2+ into rat anterior pituitary prisms and into cells of the GH3 rat anterior pituitary cell line. These responses were used as models to investigate the effects of activators and inhibitors of PKC. Depolarisation-induced 45Ca2+ influx into anterior pituitary prisms and GH3 cells was inhibited by the 'L'-type Ca2&43 channel blocker, nimodipine with equal potency in both tissues; suggesting that similar 'L'-type Ca2+ channels were being utilised in both preparations. Activators of PKC such as phorbol 12,13-dibutyrate (PDBu) and 4β-phorbol 12,13-didecanoate (4β-PDD) enhanced K+ -induced 45Ca2+ influx in anterior pituitary pieces, but inhibited K+ -induced 45Ca2+ influx into GH3 cells. The modulation seen with these phorbol esters was stereo-specific and concentration-dependent and of a similar time course in both tissues. The phorboid, mezerein, and some related phorbol esters could mimic PDBu at enhancing K+ -induced 45Ca2+ influx into anterior pituitary pieces, whereas the same compounds did not mimic the action of PDBu in GH3 cells, but instead enhanced K+ -induced 45Ca2+ influx into GH3 cells. Furthermore, the PDBu-induced enhancement of K+ -evoked 45Ca2+ influx into anterior pituitary pieces and the PDBu-induced inhibition of K+ -evoked 45Ca2+ influx into GH3 cells was reversed by the PKC inhibitors, staurosporine and H7, but not their less active congeners K252a and HA1004 respectively.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available