Fig. 8
From: Complementary roles of KCa3.1 channels and β1-integrin during alveolar epithelial repair
Expression of TRPC channels in ATII cells and complementary roles of TRPC4 and KCa3.1 in wound repair on fibronectin matrix. Representative agarose gel showing PCR products amplified from ATII cDNA with PCR primer pairs designed from rat TRPC channels (a). TRPC channel relative mRNA expressions were normalized to β-actin and compared between no coating and fibronectin matrix conditions (b, n = 16–20). c. Levels of TRPC4 protein expression in membrane fractions were measured by immunoblotting using specific anti-TRPC4 channel antibody and band intensities were compared between control (no coating) and fibronectin matrix conditions (c, right panel, n = 11). A representative immunoblot is shown in the left panel. d. ATII cells, cultured in the absence (−) or presence (+) of a fibronectin coating, were injured mechanically and the wound-healing rates (μm2/h) over a 24-h period were then compared in control condition (−), in presence of the TRPC4 inhibitor ML-204 (100 μM, +) (n = 8) or a combination of ML-204 (100 μM) and TRAM-34 (20 μM) (d, n = 7). *p < 0.05