title: In growth cones of rat cerebral neurons and human neuroblastoma cells, activation of protein kinase C causes a shift from filopodial to lamellipodial actin dynamics.
abstract: In cultures of rat cerebral neurons addition of the protein kinase C (PKC) activator 1,2-dioctanoyl-s,n-glycerol (diC8; 5 microM) induces a transient elongation of filopodia which is followed by a striking enhancement of lamellar protrusions. After 30-40 min, lamellipodia are slowly retracted, filopodia reappear and become predominant again. The reappearance of filopodia is accelerated by addition of the potent PKC-inhibitor RO-31-8220 (2 microM). A similar transient promotion of lamellar protrusive activity is obtained in SH-SY5Y neuroblastoma cells upon stimulation by acetylcholine or diC8. Immunostainings showed that the new space created by extending actin-driven lamellipodia is rapidly entered by microtubules. Preincubation with or permanent presence of RO-31-8220 totally inhibits both filopodial and lamellipodial protrusive activity. The data suggest that both filopodial and lamellipodial protrusion require active PKC, however of different levels of activation.
authors.affiliation: Institute of Zoology, University of Hohenheim-Stuttgart, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Rösner
authors.forename: H
authors.initials: H
authors.lastname: Fischer
mesh_terms: D000199:Actins / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000166:cytology / Q000201:enzymology*; D004789:Enzyme Activation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D009447:Neuroblastoma / Q000201:enzymology* / Q000473:pathology; D009474:Neurons / Q000201:enzymology*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D014407:Tumor Cells, Cultured
chemical_list: D000199:Actins; D004791:Enzyme Inhibitors; D007211:Indoles; D011493:Protein Kinase C; C064758:Ro 31-8220