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. 2014 Mar;50(3):559–570. doi: 10.1165/rcmb.2013-0258OC

Figure 4.

Figure 4.

Silencing of PKC-α subdues the cigarette smoke–driven c-Src pathway. (A) PKC-α phosphorylation was examined by immunoblots after SAE cell transfection with negative control and PKC-α siRNA and treatment with 5% CSE (0, 15, 30, 60, 90, or 120 min). (B) c-Src activation was examined after 90 minutes of CSE exposure in control or PKC-α siRNA–treated SAE cells. (C) Immunoblots for c-Src, c-Raf, and MAPK phosphorylation were conducted on cell lysate protein from SAE cells transfected with negative control and PKC-α siRNA and then treated with CSE (90 min or 24 h). (D) PKC-α phosphorylation was examined after silencing of KRAS. (E) Proposed pathway for the regulation of c-Src–mediated inflammation pathways in the lung. (F) Peripheral blood monocytes and neutrophils were examined for p-Src(Tyr416), c-Src, c-Raf, and actin after treatment with CSE (0–90 min) and AZD-0530.