Endothelin 1 (human, porcine) is a peptide vasoconstrictor and agonist of endothelin (ET) receptors ETA and ETB.
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Endothelin-1 (ET-1) is a potent vasoconstrictor peptide isolated from porcine endothelial cells[1]. Endothelin-1 (ET-1) is an astrocyte-derived signal that regulates oligodendrocyte progenitor cells (OPC) migration and differentiation. OPCs In vivo and in culture express functional ET(A) and ET(B) receptors, which mediate ET-1-induced ERK (extracellular signal-regulated kinase) and CREB (cAMP response element-binding protein) phosphorylation. ET-1 exerts both chemotactic and chemokinetic effects on OPCs to enhance cell migration; it also prevents lineage progression from the O4(+) to the O1(+) stage without affecting cell proliferation[2]. ET-1 significantly increased DNA synthesis in the cells. These biological actions were induced by ET-1, probably via a cAMP-protein kinase A pathway and intracellular calcium mobilization-protein kinase C pathway[3]. In the heart, ET-1 also causes positive inotropic and chronotropic responses and hypertrophic activity of the cardiomyocytes. ETs act via activation of two receptor subtypes, ETA and ETB receptors, both of which are coupled to various GTP-binding proteins depending on cell types[4]. The endothelin-1-induced contraction of retinal arteries is dependent on an influx of extracellular Ca2+ through membrane potential-operated calcium channels. Endothelin-1, 10-13-10-10 M, did not induce a relaxation of endothelium-intact arteries, indicating that endothelin-1 is incapable of releasing endothelium-derived relaxing factor in the retinal circulation[5]. ET-1-induced activation of PI3K/AKT is dependent on p38 mitogen-activated protein kinase (MAPK), but not extracellular signal-regulated kinase (ERK) 1/2, JNK, or transforming growth factor (TGF)-beta1. Activation of the PI3K/AKT pathway by ET-1 inhibits fibroblast apoptosis, and this inhibition is reversed by blockade of p38 MAPK or PI3K[6].
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