Endothelin 1 (swine, human), Alexa Fluor 488-labeled

Endothelin 1 (swine, human) induces reactive oxygen species, particularly superoxide anions, in vascular smooth muscle cells via the ET_A receptor signaling pathway, thereby triggering oxidative stress characterized by increased lipid peroxidation levels and decreased intracellular glutathione levels^[1].
Endothelin 1 (swine, human) promotes the synthesis of tumor necrosis factor-α in macrophages and monocytes, thereby participating in pro-inflammatory signal transduction^[1].
Endothelin 1 (swine, human) induces cyclooxygenase-2 expression and prostaglandin E₂ release in vascular endothelial cells and smooth muscle cells via the MAPK and NF-κB signaling pathways^[1].
Endothelin 1 (swine, human) enhances the expression of vascular adhesion molecules and the aggregation of polymorphonuclear neutrophils in vascular endothelial cells, thereby promoting inflammatory responses and endothelial dysfunction^[1].
Endothelin 1 (swine, human) stimulates the growth of human colorectal cancer cells, ovarian cancer cells, prostate cancer cells, Kaposi's sarcoma cells, and melanoma cell lines in vitro, with receptor dependence varying by cell type^[2].
Endothelin 1 (swine, human) acts as an autocrine growth factor for human ovarian cancer cell lines and colon cancer cell lines in vitro^[2].
Endothelin 1 (swine, human) protects rat fibroblasts, human endothelial cells and rat colon cancer cells from apoptosis^[2].
Endothelin 1 (swine, human) acts as a potent mitogen for human endothelial cells and vascular smooth muscle cells in vitro, and also promotes endothelial cell proliferation directly and indirectly by stimulating VEGF and enhancing the activity of other pro-angiogenic factors^[2].
Endothelin 1 (swine, human) stimulates the invasion and morphological differentiation of human umbilical vein endothelial cells in vitro in Matrigel by inducing the production of MMP-2^[2].
Endothelin 1 (swine, human) upregulates the expression of MMP-2 and MMP-9, and downregulates the expression of TIMP 1 and TIMP 2 in human ovarian cancer cell lines in vitro^[2].
Endothelin 1 (swine, human) blocks osteoclast-mediated bone resorption, and its production in human prostate cancer cells is enhanced upon contact with bone^[2].
Endothelin 1 (swine, human) inhibits apoptosis in cultured rat endothelial cells via an ET_B receptor-mediated pathway that is independent of phospholipase C, tyrosine kinase, MAPK, or phosphatidylinositol-3 kinase signaling pathways^[3].
Endothelin 1 (swine, human) exerts direct cytotoxic effects on cultured cardiomyocytes^[3].
Endothelin 1 (swine, human) induces cardiomyocyte hypertrophy, stimulates fibroblasts to produce type IV collagen, and alters the gene profile of cardiomyocytes by activating specific intracellular kinase cascades, thereby promoting the development of the failure phenotype^[3].

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