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Differential activation by platelet‐derived growth factor‐BB of mitogen activated protein kinases in starved or nonstarved AKR‐2B fibroblasts
Author(s) -
Hoppe Jürgen,
Hoppe Viviane,
Karenberg ThomasAndreas,
Fenn Anke,
Simm Andreas,
Sachinidis Agapios
Publication year - 1994
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041610219
Subject(s) - mitogen activated protein kinase , kinase , microbiology and biotechnology , growth factor , protein kinase a , platelet derived growth factor , chemistry , biology , biochemistry , platelet derived growth factor receptor , receptor
More than 90% of serum‐deprived (starved) AKR‐2B mouse fibroblasts are stimulated to divide by the addition of platelet‐derived growth factor (PDGF)‐BB. In density‐arrested (nonstarved) cells, PDGF‐BB affords protection from cell death without stimulation of cell division. In both cultivation conditions the cells express similar amounts of PDGF β‐receptors and the receptor kinase activity was identical as judged by its autophosphorylation capacity. Three signaling pathways were studied in detail: (1) Phospholipase C‐γ (PLC‐γ) and [Ca 2+ ]i increase, (2) activation of the phosphatidylinositol‐3 kinase (PI‐3 kinase), and (3) activation of mitogen activated kinases I and II (MAP kinases I and II). There was no difference in starved or nonstarved cells regarding PLC‐γ activation, increase of [Ca 2+ ]i, and stimulation of PL‐3 kinase activity. But most remarkably the activation of MAP‐I was largely suppressed in nonstarved cells. The implications of these signaling pathways in cell protection or cell division are discussed. © 1994 Wiley‐Liss, Inc.