scholarly journals THE ROLE OF PLACENTAL GROWTH FACTOR (PIGF) IN DIAGNOSTICS OF PREECLAMPSIA

Author(s):  
K.A. Egorova
2014 ◽  
Author(s):  
Matthew T Ratsep ◽  
Bruno Zavan ◽  
Nicki Peterson ◽  
Leandra Tolusso ◽  
Vanessa Kay ◽  
...  

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Xiaoming Deng ◽  
Ximing Xiong ◽  
Tetyana Khomenko ◽  
Longchuan Chen ◽  
Sandor Szabo ◽  
...  

Author(s):  
Elaine Colfer ◽  
Christine M. Costello ◽  
Sandro De Falco ◽  
Paul McLoughlin ◽  
Katherine Howell

2008 ◽  
Vol 48 ◽  
pp. S199-S200
Author(s):  
E. Vanheule ◽  
Y.-D. Fan ◽  
J. Van Huysse ◽  
D. Meester ◽  
M. Praet ◽  
...  

2011 ◽  
Vol 3 (2) ◽  
pp. 17-39
Author(s):  
Patrycja Sujka-Kordowska ◽  
Agnieszka Malińska ◽  
Maciej Zabel

SummaryIt is well established that angiogenesis is necessary in solid tumours development. Interesingly, the role of angiogensis in haematological malignancies has been also recognized. Recent publicationts indicate that microvessel density in bone marrow and angiogenic factors like endoglin, placental growth factor and cyclooxygenase 1 are increased in lymphoproliferative disorders and suggest that angiogensis is a part of pathomechanism of these malignancies. However, it has not been identified how angiogenesis can be involved in progression of haematological disorders. There is a strong need for further investigations in this area, since antiangiogenic therapy is a potential adjunct to conventional therapy of lymphoproliferative disorders.


2017 ◽  
Vol 36 (3) ◽  
pp. 240-246 ◽  
Author(s):  
Nokuzola Mbhele ◽  
Jagidesa Moodley ◽  
Thajasvarie Naicker

2020 ◽  
Vol 12 (572) ◽  
pp. eabc8587
Author(s):  
Yihong Chen ◽  
Anna Hultgårdh Nilsson ◽  
Isabel Goncalves ◽  
Andreas Edsfeldt ◽  
Gunnar Engström ◽  
...  

Placental growth factor (PlGF) is a mitogen for endothelial cells, but it can also act as a proinflammatory cytokine. Because it promotes early stages of plaque formation in experimental models of atherosclerosis and was implicated in epidemiological associations with risk of cardiovascular disease (CVD), PlGF has been attributed a pro-atherogenic role. Here, we investigated whether PlGF has a protective role in CVD and whether elevated PlGF reflects activation of repair processes in response to vascular stress. In a population cohort of 4742 individuals with 20 years of follow-up, high baseline plasma PlGF was associated with increased risk of cardiovascular death, myocardial infarction, and stroke, but these associations were lost or weakened when adjusting for cardiovascular risk factors known to cause vascular stress. Exposure of cultured endothelial cells to high glucose, oxidized low-density lipoprotein (LDL) or an inducer of apoptosis enhanced the release of PlGF. Smooth muscle cells and endothelial cells treated with PlGF small interference RNA demonstrated that autocrine PlGF stimulation plays an important role in vascular repair responses. High expression of PlGF in human carotid plaques removed at surgery was associated with a more stable plaque phenotype and a lower risk of future cardiovascular events. When adjusting associations of PlGF with cardiovascular risk in the population cohort for plasma soluble tumor necrosis factor–related apoptosis–inducing ligand (TRAIL) receptor-2, a biomarker of cellular stress, a high PlGF/TRAIL receptor-2 ratio was associated with a lower risk. Our findings provide evidence for a protective role of PlGF in CVD.


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