◀ Back to FGF2

FGF2 — NOS3

Text-mined interactions from Literome

Zheng et al., Endocrinology 1999 : As the mitogen activated protein kinase ( MAPK ) signal cascade has been widely associated with cell growth in response to growth factors, herein we investigate whether bFGF , EGF, and VEGF also stimulate expression of endothelial nitric oxide synthase (eNOS) via activation of the MAPK cascade in ovine fetoplacental artery endothelial cells ... Maximal stimulatory effects of bFGF and EGF on eNOS protein expression were observed at 10 ng/ml for 24 h of treatment and were associated with elevated eNOS messenger RNA ... Because treatment with all three growth factors resulted in activation of the MAPK cascade, while bFGF and EGF, but not VEGF, increased eNOS expression, we conclude that activation of the MAPK cascade is necessary, but not sufficient, for bFGF- and EGF induced increases in eNOS protein expression in ovine fetoplacental artery endothelial cells
Florio et al., Mol Pharmacol 2003 : Basic fibroblast growth factor activates endothelial nitric-oxide synthase in CHO-K1 cells via the activation of ceramide synthesis ... In these cells, the activation of eNOS by bFGF is Ca ( 2+ ) - and mitogen activated protein kinase independent ... In fact, drugs interfering with sphingomyelinase activity blocked bFGF activation of eNOS , and an increase in ceramide content was detected after bFGF treatment ... In conclusion, our data show that, in CHO-K1 cells, bFGF regulates the activity of eNOS through a novel intracellular pathway, involving the induction of ceramide synthesis and that the NO released participates in bFGF proliferative activity
Li et al., Biol Reprod 2004 : Basic fibroblast growth factor (bFGF) enhanced eNOS protein levels in static culture via a MEK mediated mechanism, but it could not further augment the elevated eNOS protein levels otherwise induced by the 15 dynes/cm2 shear stress ... The bFGF induced rise in eNOS protein levels in static culture was much less than those observed under flow and was blocked by inhibition of MEK
Li et al., Endothelium : journal of endothelial cell research 2005 : Basic fibroblast growth factor (bFGF) enhanced eNOS protein levels in static culture via a MEK mediated mechanism, but it could not further augment the elevated eNOS protein levels induced by 15 dynes/cm2 shear stress ... The bFGF induced rise in eNOS protein levels in static culture was much less than those observed under flow and was blocked by inhibiting MEK ... In conclusion, pulsatile shear stress greatly induces NO production by OFPAE cells through the mechanisms of both PI-3K mediated eNOS activation and elevations in eNOS protein levels ; bFGF does not further stimulate eNOS expression under flow condition
Mata-Greenwood et al., Placenta 2008 : Differential activation of multiple signalling pathways dictates eNOS upregulation by FGF2 but not VEGF in placental artery endothelial cells ... Herein we further investigated the temporal effects of FGF2 and VEGF on other signalling pathways including members ( Jun N-terminal kinase JNK1/2 and p38MAPK ) of mitogen activated protein kinases ( MAPK ), phosphatidylinositol-3 kinase/v-akt murine thymoma viral oncogene homologue 1 ( PI3K/AKT1 ), and the tyrosine kinase c-SRC, and examined if either one or more of these pathways play a role in the differential regulation of eNOS by FGF2 and VEGF ... We first confirmed that in oFPAE cells, FGF2 , but not VEGF, increased eNOS protein ... Thus, the FGF2 induced eNOS protein expression requires activation of multiple signalling pathways including ERK2/1, JNK1/2 and PI3K/AKT1
Kostyk et al., Am J Physiol 1995 : Basic fibroblast growth factor increases nitric oxide synthase production in bovine endothelial cells
Kunz et al., J Clin Invest 1997 : Platelet derived growth factor and fibroblast growth factor differentially regulate interleukin 1beta- and cAMP induced nitric oxide synthase expression in rat renal mesangial cells
Akiba et al., J Clin Gastroenterol 1997 (Stomach Ulcer) : Basic fibroblast growth factor increases constitutive nitric oxide synthase during healing of rat gastric ulcers