Table 1. PlGF-stimulated cellular motility is independent of de novo mRNA and protein synthesis, and inhibition of MEK/ERK pathway prevents PlGF-stimulated migration.
| Treatment | Average number of migrating cells per × 100 field±s.d. |
|---|---|
| Untreated | 4.3±2.5 |
| PlGF (1 nM) | 7.4±2.8* |
| PD98059 (50 μM) | 4.0±2.3 |
| PD98059+PlGF | 3.7±3.2 |
| LY294002 (2 μM) | 7.5±3.3* |
| LY294002+PlGF | 7.6±2.6* |
| Untreated | 8.5±3.9 |
| PlGF (1 nM) | 11.2±4.5* |
| Actinomycin D (10 μg ml−1) | 7.5±4.0 |
| Actinomycin D+PlGF | 9.5±4.1* |
| Cycloheximide (3 μg ml−1) | 7.1±4.8 |
| Cycloheximide+PlGF | 9.9±5.3* |
Abbreviations: ERK=extracellular-regulated kinase; MEK=mitogen-activated protein kinase kinase; PlGF=placental growth factor.
Five to ten × 100 fields on duplicate coverslips were evaluated for migrating cells by two researchers. Results were averaged and the s.d. was determined. The 3-h time point from two to five separate experiments is shown. *P<0.02 compared with control (PlGF vs untreated; actinomycin D+PlGF vs actinomycin D; cycloheximide+PlGF vs cycloheximide; LY294002 or LY294002+PlGF vs untreated).