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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining
J Cell Physiol 2011, PMID: 21321938

Interleukin-18/WNT1-inducible signaling pathway protein-1 signaling mediates human saphenous vein smooth muscle cell proliferation.

Reddy, Venkatapuram Seenu; Valente, Anthony J; Delafontaine, Patrice; Chandrasekar, Bysani

We demonstrate for the first time that the pro-inflammatory cytokine interleukin (IL)-18 stimulates rapid and significant proliferation of SMC derived from human saphenous vein (VSMC), but not coronary artery. IL-18 also stimulates VSMC growth. Further investigations revealed that IL-18-induced VSMC proliferation was Wnt inducible secreted protein-1 (WISP1) dependent. In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt-dependent IKK/NF-κB activation, IL-18 stimulated glycogen synthase kinase 3β phosphorylation and degradation, β-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor (TCF-LEF) activation, and WISP1 induction. Moreover, WISP1 induced its own expression, and that of survivin and multiple matrix metalloproteinases via β-catenin/TCF-LEF interaction. WISP1 also activated AP-1, but not NF-κB, and induced matrix metalloproteinase (MMP)9 transcription in part via AP-1. Interestingly, WISP1 failed to regulate tissue inhibitors of matrix metalloproteinases (TIMP) expression. These novel findings indicate that IL-18 induces a series of signaling events that result in WISP1-mediated VSMC proliferation, survival and MMP induction that are key components of vein graft stenosis and this may be amplified by IL-18 and WISP1 autoregulation and cross-regulation.

Diseases/Pathways annotated by Medline MESH: Hyperplasia
Document information provided by NCBI PubMed

Text Mining Data

TCF-LEF → WISP1: " In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction "

TCF-LEF → IL-18: " In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction "

WISP1 → glycogen synthase: " In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction "

WISP1 → IL-18: " In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction "

IKK/NF-?B → 3-kinase/Akt: " In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction "

glycogen synthase → IL-18: " In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction "

WISP1 → matrix metalloproteinase (MMP)9: " WISP1 also activated AP-1, but not NF-?B, and induced matrix metalloproteinase (MMP)9 transcription in part via AP-1 "

AP-1 → WISP1: " WISP1 also activated AP-1 , but not NF-?B, and induced matrix metalloproteinase (MMP)9 transcription in part via AP-1 "

AP-1 → matrix metalloproteinase (MMP)9: " WISP1 also activated AP-1 , but not NF-?B, and induced matrix metalloproteinase (MMP)9 transcription in part via AP-1 "

Manually curated Databases

No curated data.