Skip to main content
Fig. 5 | Skeletal Muscle

Fig. 5

From: HGF potentiates extracellular matrix-driven migration of human myoblasts: involvement of matrix metalloproteinases and MAPK/ERK pathway

Fig. 5

MAPK/ERK pathway modulation in the HGF-enhanced migration of human CHQ myoblasts. a Western blotting and densitometric analysis for ERK total (44–42 kDa) and p-ERK (44–42 kDa) in primary human CHQ myoblasts in the presence of laminin-111 (LN), fibronectin (FN), or BSA as control, and treated or not with HGF. MAPK/ERK is activated by HGF. Expression levels were normalized against the β-actin (~50 kDa) signal. Data are presented as mean ± SD. b Inhibition of p-ERK expression in human myoblasts co-treated with HGF and different concentrations of UO126 (2, 5, and 10 μM, right to left). c In the absence of HGF, the MAPK/ERK inhibitor does not modify myoblast migration towards LN-111 or FN. UO126 blocks the HGF-induced migration driven by both LN-111 and FN. Bars represent means ± SE from 4 independent experiments. *p < 0.05; ***p < 0.001

Back to article page