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. 2019 Jun 17;176(15):2736–2749. doi: 10.1111/bph.14695

Figure 6.

Figure 6

Application of exogenous PIP2 does not rescue CCL2‐evoked Ca2+ response following DAG kinase inhibition, but inhibition is mimicked by OAG in THP‐1 cells. (a) CCL2‐evoked (50 ng·ml−1) intracellular Ca2+ responses in the presence of vehicle control (closed circles), R59949 (open circles; 30 μM), or R59949 plus exogenous PIP2 (squares; 300 μM; n = 8). (b) Bar chart showing average peak intracellular Ca2+ responses. *P < .05 versus vehicle control. (c) CCL2‐evoked (50 ng·ml−1) intracellular Ca2+ responses in the presence of vehicle control (closed circles) or cell permeable DAG analogue, OAG (open circles; n = 8). (d) Concentration–inhibition curve for OAG effect on intracellular Ca2+ responses evoked by CCL2 (50 ng·ml−1; n = 8). (e) Effect of OAG (30 μM) on CCL2 concentration–response curve in THP‐1 cells (IC50 9 ± 1 μM; n = 6). Responses are in the presence of vehicle control (closed circles) or OAG (open circles). F ratio is the Ca2+ response as measured by the Fura‐2 emission intensity ratio when excited at 340 and 380 nm. Data in inhibition experiments are expressed as a percentage of the control response in the presence of vehicle alone