[The role of intermediate filaments in forming cellular processes induced in fibroblasts by the tumor promoter TPA].
A tumor promoter phorbol 12-myristate 13-acetate (PMA) induces characteristic reversible changes in the cell shape in certain fibroblastic lines. This reaction to PMA may be regarded as a prototype of reorganizations involving formation of stable cytoplasmic processes. Two specific drugs, Taxol and Colcemid, were used to study the role of microtubules and vimentin-containing intermediate filaments (IF) in the development of PMA-induced reorganizations. A short (I h) exposure to PMA induced formation of processes in the control cells rather than in the Colcemid treated cells having depolymerized microtubules and the IF that collapsed around the nucleus. A longer (3-4 h) exposure to PMA of the colcemid-treated cells induced a partial reversal of the IF collapse; those parts of peripheral lamellae that contained IF were transformed into narrow noncontractile processes. It is suggested that the local interaction of the IF with the actin system is an essential step in the formation of processes from lamellae.
A D
AD
Bershadskiĭ
O Iu
OIu
Ivanova
L A
LA
Liass
O Iu
OIu
Pletiushkina
Iu M
IuM
Vasil'ev
I M
IM
Gel'fand
D000199:Actins / Q000187:drug effects / Q000648:ultrastructure; D000470:Alkaloids / Q000494:pharmacology; D000818:Animals; D002461:Cell Line, Transformed; D002478:Cells, Cultured / Q000187:drug effects / Q000648:ultrastructure; D003703:Demecolcine / Q000494:pharmacology; D004347:Drug Interactions; D005347:Fibroblasts / Q000187:drug effects* / Q000648:ultrastructure; D005455:Fluorescent Antibody Technique; D007382:Intermediate Filaments / Q000187:drug effects* / Q000648:ultrastructure; D051379:Mice; D008870:Microtubules / Q000187:drug effects / Q000648:ultrastructure; D017239:Paclitaxel; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D000199:Actins; D000470:Alkaloids; D013755:Tetradecanoylphorbol Acetate; D017239:Paclitaxel; D003703:Demecolcine
Rol' promezhutochnykh filamentov v formirovanii kletochnykh otrostkov, indutsirovannykh u fibroblastov opukholevym promotorom TFA.