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Title:
PDGF-CC induces tissue factor expression: role of PDGF receptor α/β | Basic Research in Cardiology
Description:
Tissue factor (TF) is the principal trigger of the coagulation cascade and involved in arterial thrombus formation. Platelet-derived growth factor CC (PDGF-CC) is a recently discovered member of the PDGF family released upon platelet activation. This study assesses the impact of PDGF-CC on TF expression in human cells. PDGF-CC concentration-dependently induced TF expression by 2.5-fold in THP-1 cells, by 2.0-fold in human peripheral blood monocytes, by 1.4-fold in vascular smooth muscle cells, and by 2.6-fold in microvascular endothelial cells, but did not affect TF expression in aortic endothelial cells. A similar pattern was observed with PDGF-BB. In contrast, PDGF-AA did not alter TF expression in THP-1 cells. TF whole cell activity was induced following stimulation with PDGF-BB and PDGF-CC in THP-1 cells. Real-time polymerase chain reaction revealed that PDGF-CC induced TF mRNA. PDGF-CC transiently activated p42/44 MAP kinase [extracellular signal-regulated kinase (ERK)], while phosphorylation of the MAP kinases c-Jun NH2-terminal kinase (JNK) and p38 remained unaffected. PD98059, a specific inhibitor of ERK phosphorylation, but not the p38 inhibitor SB203580 or the JNK inhibitor SP600125 prevented PDGF-CC induced TF expression in a concentration-dependent manner. The effect of PDGF-CC was antagonized by both PDGF receptor α and PDGF receptor β neutralizing antibodies; in contrast, PDGF-BB was only inhibited by PDGF receptor β blocking antibody. PDGF receptor α and PDGF receptor β inhibition prevented PDGF-CC-induced ERK phosphorylation. PDGF-CC induces TF expression via activation of α/β receptor heterodimers and an ERK-dependent signal transduction pathway.
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Keywords {🔍}
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Topics {✒️}
platelet-derived growth factor-bb mitogen-activated protein kinase mitogen-activated protein kinases platelet-derived growth factor month download article/chapter human monocyte-derived macrophages pdgf receptor α/β α/β receptor heterodimers growth factor stimulation inhibits tissue factor tissue factor expression platelet-vessel wall interactions adenovirus-encoded hammerhead ribozyme growth factor express tissue factor soluble tissue factor tissue factor synthesis tissue factor antigen article basic research aortic endothelial cells receptors transiently delays beta receptor microvascular endothelial cells pdgf receptor α vascular smooth muscle protease-activated ligand full article pdf pdgf-receptor-alpha pdgf alpha-receptor concentration-dependent manner related subjects tissue factor arterial thrombus formation vascular expression patterns stromal pdgf receptors badimon privacy choices/manage cookies affect tf expression alter tf expression platelet alpha granules cell activity p38 inhibitor sb203580 endotoxin-induced effects human vascular smcs tissue plasminogen activator pdgf family released pdgf family member erk kinases arterial thrombosis pdgf-cc
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headline:PDGF-CC induces tissue factor expression: role of PDGF receptor α/β
description:Tissue factor (TF) is the principal trigger of the coagulation cascade and involved in arterial thrombus formation. Platelet-derived growth factor CC (PDGF-CC) is a recently discovered member of the PDGF family released upon platelet activation. This study assesses the impact of PDGF-CC on TF expression in human cells. PDGF-CC concentration-dependently induced TF expression by 2.5-fold in THP-1 cells, by 2.0-fold in human peripheral blood monocytes, by 1.4-fold in vascular smooth muscle cells, and by 2.6-fold in microvascular endothelial cells, but did not affect TF expression in aortic endothelial cells. A similar pattern was observed with PDGF-BB. In contrast, PDGF-AA did not alter TF expression in THP-1 cells. TF whole cell activity was induced following stimulation with PDGF-BB and PDGF-CC in THP-1 cells. Real-time polymerase chain reaction revealed that PDGF-CC induced TF mRNA. PDGF-CC transiently activated p42/44 MAP kinase [extracellular signal-regulated kinase (ERK)], while phosphorylation of the MAP kinases c-Jun NH2-terminal kinase (JNK) and p38 remained unaffected. PD98059, a specific inhibitor of ERK phosphorylation, but not the p38 inhibitor SB203580 or the JNK inhibitor SP600125 prevented PDGF-CC induced TF expression in a concentration-dependent manner. The effect of PDGF-CC was antagonized by both PDGF receptor α and PDGF receptor β neutralizing antibodies; in contrast, PDGF-BB was only inhibited by PDGF receptor β blocking antibody. PDGF receptor α and PDGF receptor β inhibition prevented PDGF-CC-induced ERK phosphorylation. PDGF-CC induces TF expression via activation of α/β receptor heterodimers and an ERK-dependent signal transduction pathway.
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Cardiology
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description:Tissue factor (TF) is the principal trigger of the coagulation cascade and involved in arterial thrombus formation. Platelet-derived growth factor CC (PDGF-CC) is a recently discovered member of the PDGF family released upon platelet activation. This study assesses the impact of PDGF-CC on TF expression in human cells. PDGF-CC concentration-dependently induced TF expression by 2.5-fold in THP-1 cells, by 2.0-fold in human peripheral blood monocytes, by 1.4-fold in vascular smooth muscle cells, and by 2.6-fold in microvascular endothelial cells, but did not affect TF expression in aortic endothelial cells. A similar pattern was observed with PDGF-BB. In contrast, PDGF-AA did not alter TF expression in THP-1 cells. TF whole cell activity was induced following stimulation with PDGF-BB and PDGF-CC in THP-1 cells. Real-time polymerase chain reaction revealed that PDGF-CC induced TF mRNA. PDGF-CC transiently activated p42/44 MAP kinase [extracellular signal-regulated kinase (ERK)], while phosphorylation of the MAP kinases c-Jun NH2-terminal kinase (JNK) and p38 remained unaffected. PD98059, a specific inhibitor of ERK phosphorylation, but not the p38 inhibitor SB203580 or the JNK inhibitor SP600125 prevented PDGF-CC induced TF expression in a concentration-dependent manner. The effect of PDGF-CC was antagonized by both PDGF receptor α and PDGF receptor β neutralizing antibodies; in contrast, PDGF-BB was only inhibited by PDGF receptor β blocking antibody. PDGF receptor α and PDGF receptor β inhibition prevented PDGF-CC-induced ERK phosphorylation. PDGF-CC induces TF expression via activation of α/β receptor heterodimers and an ERK-dependent signal transduction pathway.
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PDGF
Monocytes
Microvascular endothelial cells
Arterial thrombosis
Cardiology
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