Skip to main content
. 2013 Jul 2;14(8):726–732. doi: 10.1038/embor.2013.89

Figure 3.

Figure 3

The A3AR-selective antagonist MRS1334 and cytochalasin B inhibit A3AR agonist-stimulated cytoneme formation. (A) The A3AR-selective agonist 2-Cl-IB-MECA (1 μM at t=0 s) promotes the extension of cytonemes from neutrophils. Quantitative analysis revealed that 2-Cl-IB-MECA treatment significantly increases the percentage of cells exhibiting cytonemes (B) and the number of cytonemes/cell (C), effects inhibited by MRS1334 or cytochalasin B. Data shown are means±s.e.m. of 26–35 individual experiments; significance was determined via one-way analysis of variance with post-hoc Newman–Keuls tests. (D) ATRA-differentiated HL60 cells, which exhibited both A3AR plaques and plaque-associated cytonemes (merged image of a Vybrant DiO and CA200645-labelled HL60 cell), were transfected with the fluorescent F-actin probe LifeAct, confirming the presence of F-actin in these structures (inlay, white). **P<0.01, ***P<0.001. A3AR, A3-adenosine receptor; HBSS, Hank’s Buffered Salt Solution; 2-Cl-IB-MECA, 2-chloro-N6-(3-iodobenzyl)adenosine-5′-N-methylcarboxamide.