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. 2001 Feb 15;21(4):1274–1282. doi: 10.1523/JNEUROSCI.21-04-01274.2001

Table 1.

Expression of cyclins and cyclin-dependent kinases in oligodendrocyte progenitor cells changes during development in culture and after treatment with agents that cause cell cycle arrest in G1 phase

Relative protein levels (% of PDGF-treated controls)
Culture conditions Cell cycle withdrawal Cell cycle arrest
N1 T3 iso kai TEA ver
Cyclin D 40  ± 10* 41  ± 8* 166  ± 21* 198  ± 8.01-168 144  ± 12* 177  ± 9.2*
Cyclin E 15  ± 41-160 44  ± 161-165 117  ± 9.9 104  ± 2.6 108  ± 20 114  ± 16
Cdk2 78  ± 6.7* 69  ± 7.8* 112  ± 5.0 98  ± 5.3 81  ± 9.5 94  ± 6.0
Cdk4 79  ± 8.1* 65  ± 4.21-165 106  ± 2.9 106  ± 9.5 80  ± 15 90  ± 2.5
Cdk6 58  ± 15* 20  ± 7.91-165 105  ± 6.5 125  ± 20 121  ± 18 127  ± 25

OP cells were cultured under conditions that caused permanent cell cycle withdrawal (2 d in PDGF, followed by 3 d in N1 plus 0.5% FBS medium or N1 plus T3 hormone medium) or reversible cell cycle arrest in G1 phase [2 d in PDGF, in the presence or in the absence of the β-AR agonist isoproterenol (iso; 50 μm), the GluR agonist kainate (kai; 100 μm), the K+ channel blocker TEA (5 mm), or the Na+ channel opener veratridine (ver; 30 μm)]. Western blot analysis was performed by loading 20–25 μg of cell lysates for each sample. Values were determined by densitometric analysis of autoradiographs from Western blots and are expressed as ratios of samples treated with PDGF alone. The mean ± SEM of three to five separate experiments is shown for each treatment;

*

p < 0.05,

F1-160: p < 0.01,

F1-165: p< 0.005, and

F1-168: p < 0.001 compared with PDGF-treated cells (Student's t test).