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. 2017 Sep 22;15:433–446. doi: 10.1016/j.csbj.2017.09.002

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© 2017 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Fig. 4 — Signaling pathways affected by PP13

A scheme of the endothelium-dependent vascular relaxation pathways developed according to Drobnjak et al., Ref. [129]. Interaction of PP13 with the endothelial layer results in activation of nitric oxide (NO) production via endothelial nitric oxide synthase (eNOS), as well as metabolism of arachidonic acid (AA) to prostaglandins (PG) via cyclooxygenase (COX1/2) enzymes. NO and PG normally elicit relaxation of vascular smooth muscle cells through cGMP and cAMP, respectively. The endothelial element activated by PP13 is yet unknown. Note that, in the context of blood vessel relaxation, PP13 does not alter endothelial cytosolic Ca^2 + levels, and that the IP (prostacyclin) receptor is not involved, suggesting that another prostaglandin, e.g. prostaglandin E2 (PGE2) may be responsible.

cAMP (cyclic adenosine monophosphate), cGMP (cyclic guanosine monophosphate), PLA₂ (phospholipase A2), PLC (phospholipase C), PGE2 (prostaglandin E2), PGH2 (prostaglandin H2), PGi2 (prostacyclin 2), TXA2 (thromboxane 2). Scheme adapted from Drobnjak et al., Ref. [129].