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. 2021 Jun 22;6(12):e142945. doi: 10.1172/jci.insight.142945

Figure 6. Activation of α7 nAChR results in Ca2+-mediated EGFR transactivation.

Figure 6

(A) Averaged time course of the changes in [Ca2+]c in ARCF in response to 600 nM nicotine treatment (added at 30 seconds) in the presence (red squares, n = 63) or absence of 100 nM α-BTX (blue circles, n = 34). Data normalized to before nicotine stimulation. (B) EGFR transactivation in HEK293T overexpressing EGFR, α7 nAChR, and NACHO in presence of a cell-permeable Ca2+ chelator BAPTA-AM. (C) Summary data from B (n = 8). (D) Proposed mechanism of α7 nAChR–activated proliferation and enhanced collagen content in CF. Data are shown as mean ± SEM. ANOVA followed by Bonferroni comparison. *P < 0.05. ACh, acetylcholine; α-BTX, α-bungarotoxin; nAChR, nicotinic acetylcholine receptor; BAPTA, 1;2-bis(o-aminophenoxy)ethane-N;N;N′;N′-tetraacetic acid.