scholarly journals Antagonis Soluble Fms-Like Tyrosine Kinase 1 (sFlt-1) dan Soluble Endoglin (sEng) pada Preeklamsia

2017 ◽  
Vol 4 (1) ◽  
pp. 1
Author(s):  
Mohd Andalas ◽  
Harahap Harahap
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
Tissue Growth ◽  
Placental Growth Factor ◽  
Angiogenic Factor ◽  
Main Role ◽  
Vascular Endothelial ◽  
Vascular Health ◽  
Soluble Endoglin ◽  
Endothelial Growth Factor

Proangiogenic factor signal transduction like vascular endothelial growth factor (VEGF), placental growth factor(PlGF) and tissue growth factor â-1 (TGFâ-1) are important to angiogenesis and vascular health in pregnancy. Inpreeclampsia (PE) concentration of fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng) are increasesignificantly. Base on analysis from resent research shown that sFlt-1 and sEng inhibit angiogenic factor signaltransduction by competition - in result angiogenic factor can‘t bind to their receptor. sFlt-1 and sEng are potential usedas preeclampsia therapy because sFlt-1 and sEng have main role in PE pathogenesis. We suggest that the research tofind out effective sFlt-1 and sEng antagonist have to conduct in the next time.

scholarly journals Angiogenic factors and pre-eclampsia: an early marker is needed

2009 ◽  
Vol 116 (3) ◽  
pp. 231-232 ◽  
Author(s):  
Holger Stepan
Keyword(s):  
Growth Factor ◽  
Normal Pregnancy ◽  
Pregnancy Complication ◽  
Placental Growth Factor ◽  
Angiogenic Factors ◽  
Vascular Endothelial ◽  
Alternative Splice Variant ◽  
Soluble Endoglin ◽  
Endothelial Growth Factor

Pre-eclampsia, a pregnancy complication characterized by hypertension and proteinuria, is still a major cause of neonatal and maternal mortality, and acute and long-term morbidities for both mother and neonate. There is mounting evidence that an imbalance between angiogenic factors, such as VEGF (vascular endothelial growth factor) or PlGF (placental growth factor), and factors inhibiting angiogenesis, such as sFlt1 (soluble fms-like tyrosine kinase 1) and sEng (soluble endoglin), are closely related to the pathogenesis of pre-eclampsia. In the present issue of Clinical Science, Bills and co-workers report that VEGF165b, an alternative splice variant of the VEGF pre-mRNA, is up-regulated in women with normal pregnancy and that this increase was delayed or diminished in women who developed pre-eclampsia. Thus this protein could serve (alone or in combination with other parameters) as a new marker for risk assessment in terms of pre-eclampsia.

Upregulation of angiotensin-converting enzyme by vascular endothelial growth factor

2001 ◽  
Vol 280 (2) ◽  
pp. H885-H891 ◽  
Author(s):  
Outi Saijonmaa ◽  
Tuulikki Nyman ◽  
Riikka Kosonen ◽  
Frej Fyhrquist
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Angiotensin Converting Enzyme ◽  
Tyrosine Kinase ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Converting Enzyme ◽  
Endothelial Growth Factor

The role of vascular endothelial growth factor (VEGF), a potent endothelium-specific angiogenic factor, in the regulation of angiotensin-converting enzyme (ACE) in cultured human umbilical vein endothelial cells (HUVECs) was studied. VEGF (0.07–1.2 × 10−6mmol/l) caused a dose-dependent increase in ACE measured in intact endothelial cells and increased the expression of ACE mRNA. The stimulatory effect of VEGF was inhibited by pretreatment of endothelial cells with the tyrosine kinase inhibitor herbimycin (4.35 × 10−5mmol/l). The stimulatory effect of VEGF was potentiated by the selective cGMP phosphodiesterase inhibitor zaprinast (0.1 mmol/l). The nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME; 5.4 mmol/l) suppressed the stimulatory effect of VEGF. The nonselective cyclooxygenase (COX) inhibitor indomethacin (5 μM) and the selective COX-2 inhibitor NS-398 (5 μM) potentiated the stimulatory effect of VEGF, whereas the selective COX-1 inhibitor resveratrol (5 μM) was without effect. ACE induction by VEGF was inhibited by the selective protein kinase C (PKC) inhibitor GF109203X (2.5 × 10−3mmol/l) and by downregulating PKC with phorbol 12-myristate 13-acetate. In summary, VEGF induced ACE in cultured HUVECs. Intracellular events such as tyrosine kinase activation, PKC activation, and increase of cGMP were probably involved in ACE induction by VEGF. Nitric oxide may partially contribute to ACE induction by VEGF. The powerful capacity of VEGF to increase ACE in endothelial cells shown here suggests a synergistic relation between VEGF and the renin-angiotensin system in vascular biology and pathophysiology.

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