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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Pharmacol Res. 2020 Nov 4;163:105272. doi: 10.1016/j.phrs.2020.105272

Figure 5: The rapid V2R-induced angiopoietin-2 upregulation is mediated by PLCB and not by the activation of MAPK pathway.

Figure 5:

(A) A screening G-protein-coupled multi-gene assay targeting 38 genes suggested that PLCB4 expression was significantly elevated by 2-hour-long V2R stimulation. (B, C, D, and E) The lack of influence of the MAPK pathway and the PLCB4 upregulation was confirmed with DDAVP and MRSA treatment during 0.5, 1, 3, and 6 hours, n=3 for each group. (D) After 3 hours of treatment, we observed a slight increase in PLCB4 expression with both MRSA and DDAVP challenge and parallel to an increase in ANGPT2 (angiopoietin-2 gene) expression. (E) The PLCB4 upregulation was significant after 6 hours of DDAVP treatment. In a subsequent experiment, cells were treated with U73122, a pharmacological inhibitor of PLCB, before the addition of DDAVP. As shown, (F) treatment with U73122 prevents the DDAVP-induced upregulation of ANGPT2. Data are expressed as mean ± SD. *p <0.05 vs. Vehicle.