Novel Cross-Talk between Three Cardiovascular Regulators: Thrombin Cleavage Fragment of Jagged1 Induces Fibroblast Growth Factor 1 Expression and Release

被引:17
作者
Duarte, Maria [1 ]
Kolev, Vihren [1 ]
Kacer, Doreen [1 ]
Mouta-Bellum, Carla [1 ]
Soldi, Raffaella [1 ]
Graziani, Irene [1 ]
Kirov, Aleksandr [1 ]
Friesel, Robert [1 ]
Liaw, Lucy [1 ]
Small, Deena [2 ]
Verdi, Joseph [1 ]
Maciag, Thomas [1 ]
Prudovsky, Igor [1 ]
机构
[1] Maine Med Ctr, Res Inst, Ctr Mol Med, Scarborough, ME 04074 USA
[2] Univ New Hampshire, Dept Mol Cellular & Biomed Sci, Durham, NH 03824 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1091/mbc.E07-12-1237
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Angiogenesis is controlled by several regulatory mechanisms, including the Notch and fibroblast growth factor (FGF) signaling pathways. FGF1, a prototype member of FGF family, lacks a signal peptide and is released through an endoplasmic reticulum-Golgi-independent mechanism. A soluble extracellular domain of the Notch ligand Jagged1 (sJ1) inhibits Notch signaling and induces FGF1 release. Thrombin, a key protease of the blood coagulation cascade and a potent inducer of angiogenesis, stimulates rapid FGF1 release through a mechanism dependent on the major thrombin receptor protease-activated receptor (PAR) 1. This study demonstrates that thrombin cleaves Jagged1 in its extracellular domain. The sJ1 form produced as a result of thrombin cleavage inhibits Notch-mediated CBF1/Suppressor of Hairless [(Su(H)]/Lag-1-dependent transcription and induces FGF1 expression and release. The overexpression of Jagged1 in PAR1 null cells results in a rapid thrombin-induced export of FGF1. These data demonstrate the existence of novel cross-talk thrombin, FGF, and Notch signaling pathways, which play important roles in vascular formation and remodeling.
引用
收藏
页码:4863 / 4874
页数:12
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