Figure 2: Adenosine mediates increase in IL-1β via the A2A receptor and amplifies signal 1 and signal 2 pathways. | Nature Communications

Figure 2: Adenosine mediates increase in IL-1β via the A2A receptor and amplifies signal 1 and signal 2 pathways.

From: Adenosine is required for sustained inflammasome activation via the A2A receptor and the HIF-1α pathway

Figure 2

(a) LPS-primed PECs were treated with NECA (10 μM) in the presence or absence of three different adenosine receptor antagonists for A1 (DPCPX, 10 nM), A2A (ZM241385, 10 μM), A2B (MRS1706, 10 nM), A3 (MRS1523, 5 μM) or their combinations for 1 h and were pulsed with ATP for 20 min. (b) A2A receptor-specific agonist (CGS21680) and antagonist ZM241385 increase and block IL-1β production, respectively. (c) LDH release in PECs showed no difference in the presence or absence of ZM241385 as sampled from b. (d) PECs from A2A receptor-deficient cells have low IL-1β production, which is not increased by NECA and CGS21680. (e) CGS21680 increases the induction of Il1b mRNA expression, and this was decreased in A2A receptor-deficient cells. (f) Loss of the A2A receptor in macrophages results in much lower levels of Il1b mRNA expression in response to LPS. (g) CGS21680 and ZM241385 increase and decrease production of cleaved caspase-1. (h) The production of cleaved caspase-1 is decreased in A2A receptor-deficient macrophages. Data are expressed as the mean±s.d. from at least three independent experiments. Immunoblots shown are representative results from at least three independent experiments. *P<0.05 determined by Student’s t-test.

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