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Figure 4. Stretch-induced ERK phosphorylation in hGF. (A) hGF were cultured in serum-free conditions for 24 hrs prior to being stretched for the indicated times (in min). A 20-µg quantity of total cellular proteins was separated by SDS-PAGE, transferred to nitrocellulose, and probed with phospho-specific ERK1,2 antibody (upper panel) or total ERK1,2 antibody (lower panel). + = positive control, MC3T3-E1 mouse osteoblast cell line [ERK1, 44 kDa; ERK2, 42 kDa].

Stretch and serum cause increased PCNA expression in hGF. (B) hGF were stretched in serum-free medium for the times indicated (in hrs). A 20-µg quantity of total cellular proteins was separated by SDS-PAGE, transferred to nitrocellulose, and probed with anti-PCNA antibody (upper panel) or actin antibody (lower panel). PC, positive control; hGF cultured in 10% FBS-containing medium for 24 hrs. (C) Densitometric analysis of PCNA normalized to β-actin for two independent stretch experiments (represented as fold induction over static condition at each time point; N = 2; 24 hrs, 1.98 ± 0.233; 48 hrs, 1.16 ± 0.01). (D) hGF were cultured in serum-free medium for 24 hrs prior to stimulation with 10 ng/mL PDGF for 24 or 48 hrs as indicated. A 20-µg quantity of total cellular proteins was separated by SDS-PAGE, transferred to nitrocellulose, and probed with anti-PCNA antibody (upper panel) or actin antibody (lower panel).

J DENT RES, Vol. 83, No. 8, 596-601 (2004)
DOI: 10.1177/154405910408300803

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