n-(2-carboxyethyl)pyrrole and Inflammation

n-(2-carboxyethyl)pyrrole has been researched along with Inflammation* in 1 studies

Other Studies

1 other study(ies) available for n-(2-carboxyethyl)pyrrole and Inflammation

Article	Year
Oxidative stress induces angiogenesis by activating TLR2 with novel endogenous ligands. Nature, 2010, Oct-21, Volume: 467, Issue:7318 Reciprocity of inflammation, oxidative stress and neovascularization is emerging as an important mechanism underlying numerous processes from tissue healing and remodelling to cancer progression. Whereas the mechanism of hypoxia-driven angiogenesis is well understood, the link between inflammation-induced oxidation and de novo blood vessel growth remains obscure. Here we show that the end products of lipid oxidation, ω-(2-carboxyethyl)pyrrole (CEP) and other related pyrroles, are generated during inflammation and wound healing and accumulate at high levels in ageing tissues in mice and in highly vascularized tumours in both murine and human melanoma. The molecular patterns of carboxyalkylpyrroles are recognized by Toll-like receptor 2 (TLR2), but not TLR4 or scavenger receptors on endothelial cells, leading to an angiogenic response that is independent of vascular endothelial growth factor. CEP promoted angiogenesis in hindlimb ischaemia and wound healing models through MyD88-dependent TLR2 signalling. Neutralization of endogenous carboxyalkylpyrroles impaired wound healing and tissue revascularization and diminished tumour angiogenesis. Both TLR2 and MyD88 are required for CEP-induced stimulation of Rac1 and endothelial migration. Taken together, these findings establish a new function of TLR2 as a sensor of oxidation-associated molecular patterns, providing a key link connecting inflammation, oxidative stress, innate immunity and angiogenesis. Topics: Aging; Animals; Aorta; Cell Line; Cell Movement; Endothelial Cells; Hindlimb; Humans; Immunity, Innate; Inflammation; Ischemia; Ligands; Melanoma; Mice; Mice, Inbred C57BL; Myeloid Differentiation Factor 88; Neovascularization, Pathologic; Neovascularization, Physiologic; Oxidation-Reduction; Oxidative Stress; Platelet Endothelial Cell Adhesion Molecule-1; Propionates; Pyrroles; rac1 GTP-Binding Protein; Receptors, Scavenger; Signal Transduction; Toll-Like Receptor 2; Toll-Like Receptor 4; Vascular Endothelial Growth Factor A; Wound Healing	2010

Article

Year

Oxidative stress induces angiogenesis by activating TLR2 with novel endogenous ligands.

Nature, 2010, Oct-21, Volume: 467, Issue:7318

Reciprocity of inflammation, oxidative stress and neovascularization is emerging as an important mechanism underlying numerous processes from tissue healing and remodelling to cancer progression. Whereas the mechanism of hypoxia-driven angiogenesis is well understood, the link between inflammation-induced oxidation and de novo blood vessel growth remains obscure. Here we show that the end products of lipid oxidation, ω-(2-carboxyethyl)pyrrole (CEP) and other related pyrroles, are generated during inflammation and wound healing and accumulate at high levels in ageing tissues in mice and in highly vascularized tumours in both murine and human melanoma. The molecular patterns of carboxyalkylpyrroles are recognized by Toll-like receptor 2 (TLR2), but not TLR4 or scavenger receptors on endothelial cells, leading to an angiogenic response that is independent of vascular endothelial growth factor. CEP promoted angiogenesis in hindlimb ischaemia and wound healing models through MyD88-dependent TLR2 signalling. Neutralization of endogenous carboxyalkylpyrroles impaired wound healing and tissue revascularization and diminished tumour angiogenesis. Both TLR2 and MyD88 are required for CEP-induced stimulation of Rac1 and endothelial migration. Taken together, these findings establish a new function of TLR2 as a sensor of oxidation-associated molecular patterns, providing a key link connecting inflammation, oxidative stress, innate immunity and angiogenesis.

Topics: Aging; Animals; Aorta; Cell Line; Cell Movement; Endothelial Cells; Hindlimb; Humans; Immunity, Innate; Inflammation; Ischemia; Ligands; Melanoma; Mice; Mice, Inbred C57BL; Myeloid Differentiation Factor 88; Neovascularization, Pathologic; Neovascularization, Physiologic; Oxidation-Reduction; Oxidative Stress; Platelet Endothelial Cell Adhesion Molecule-1; Propionates; Pyrroles; rac1 GTP-Binding Protein; Receptors, Scavenger; Signal Transduction; Toll-Like Receptor 2; Toll-Like Receptor 4; Vascular Endothelial Growth Factor A; Wound Healing

2010