Placenta Growth Factor: Identification and Characterization of a Novel Isoform Generated by RNA Alternative Splicing

Cao, Yang; Wr, Ji; Qi, Peng; Rosin, Åsa

doi:10.1006/bbrc.1997.6813

Cited by 168 publications

(114 citation statements)

References 27 publications

Supporting

Mentioning

108

Contrasting

Unclassified

Order By: Relevance

“…PlGF has three spliced forms, PlGF-1, PlGF-2, and PlGF-3 (31,32). In the rhesus monkey, where three early stages of pregnancy (lacunar, early villous, and villous PL stages) were studied for PlGF expression by immunohistology (33), weak, transient stromal expression was found on vascular smooth muscle cells and glandular epithelium.…”

Section: Discussionmentioning

confidence: 99%

Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Tayade

Hilchie

et al. 2007

The Journal of Immunology

110

View full text Add to dashboard Cite

Placenta growth factor (PlGF; formerly PGF), a vascular endothelial growth factor gene family member, is expressed in human implantation sites by maternal uterine NK (uNK) and fetal trophoblast cells. Lower than normal concentrations of blood and urinary PlGF have been associated with impending onset of pre-eclampsia, a hypertensive disease of late human gestation characterized by limited intravascular trophoblast invasion. In pregnant rodents, delivery of the PlGF antagonist sFlt-1 or S-endoglin induces pre-eclampsia-like lesions. Mice genetically deleted in PlGF reproduce, but neither their implantation sites nor their uNK cell development are described. We combined real-time PCR of endometrium from nonpregnant and gestation day (gd)6–18 C57BL6/J (B6) mice with immunohistology to analyze PlGF expression in normal mouse pregnancy. To estimate the significance of uNK cell-derived PlGF, PlGF message was quantified in mesometrial decidua from pregnant alymphoid Rag2 null/common γ chain null mice and in laser capture-microdissected B6 uNK cells. Histopathologic consequences from PlGF deletion were also characterized in the implantation sites from PlGF null mice. In B6, decidual PlGF expression rose between gd8–16. uNK cells were among several types of cells transcribing PlGF in decidualized endometrium. Immature uNK cells, defined by their low numbers of cytoplasmic granules, were the uNK cells displaying the greatest number of transcripts. PlGF deletion promoted the early differentiation high numbers of binucleate uNK cells (gd8) but had no other significant, morphometrically detectable impact on implantation sites. Thus, in mice, PlGF plays an important role in successful uNK cell proliferation and/or differentiation.

show abstract

Section: Discussionmentioning

confidence: 99%

Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Tayade

Hilchie

et al. 2007

The Journal of Immunology

110

View full text Add to dashboard Cite

show abstract

“…It is well accepted that the angiogenic growth factors VEGF and PlGF exist in placenta and act as important factors for placental development and fetal growth [8,23]. PlGF is abundantly expressed in the trophoblast cells of pla- centa [4,13,23]. We previously reported the expression and distribution of PlGF mRNA in the rat placenta at various gestational phases [7].…”

Section: Discussionmentioning

confidence: 99%

Streptozotocin-Induced Diabetes Decreases Placenta Growth Factor (PIGF) Levels in Rat Placenta

Koh

Sung

Won

et al. 2007

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

ABSTRACT. The placenta produces several growth factors, including placenta growth factor (PlGF), which are essential for placenta growth and fetal growth. Diabetic pregnancy induces the abnormal placental growth and fetal development. This study investigated whether diabetes in pregnant rats induces changes in PlGF expression in the placenta. Diabetes was induced by a single intravenous injection of streptozotocin (35 mg/kg body weight) on day 0 of pregnancy, blood and tissue samples were collected on day 20 of pregnancy. In the diabetic group, maternal body weight and fetal weight significantly decreased compared to controls. RT-PCR and Western blot analyses showed that expression of PlGF was significantly decreased in placenta by streptozotocin treatment. Immunohistochemical study showed that the positive signal of PlGF in trophoblast cells was decreased in the diabetic group compared to controls. These findings demonstrate the decline of PlGF in the placenta in diabetic pregnancy. KEY WORDS: diabetes, placenta, PlGF.J. Vet. Med. Sci. 69(9): 877-880, 2007 The placenta is a critical organ for both fetal development and the maintenance of pregnancy. Growth of the placenta is regulated by several growth factors, including placental growth factor (PlGF), vascular endothelial growth factor (VEGF), and fibroblast growth factor-2 [1, 14, 15]. These growth factors are responsible for fetal development as well as placenta growth [5,9,20,22]. PlGF is a polypeptide growth factor that shares a 53% amino acid sequence homology with the platelet-derived growth factor domain of VEGF [17]. Unlike VEGF, abundant expression of PlGF is restricted to the placenta [18]. PlGF was formerly known as a potent angiogenic growth factor capable of inducing the proliferation, migration, and activation of endothelial cells [17]. PlGF plays an important endocrinological and nutritional role, and contributes to the regulation of placental function.Gestational diabetes is one of the most common complications of pregnancy, and is associated with both abnormal placental growth and fetal development [3,16,19]. Severely diabetic pregnancy can induce abortion and prematurity [3,19]. Recently, apoptotic cell death was increased in the placenta of pregnant women with gestational diabetes [21]. PlGF acts as an anti-apoptotic factor for trophoblast in vitro [11]. Therefore, we propose that diabetic pregnancy induces change in PlGF expression and this dysregulation may affect placental development. However, little data is available on the expression of PlGF in the placenta tissue in diabetic pregnancy. Therefore, the present study was performed to provide this information. MATERIALS AND METHODSExperimental animals: Female Sprague-Dawley rats (200-220 g, n=30) were purchased from Samtako Co. (Laboratory Animal Breeding Center, Korea), randomly divided into 2 groups, control group and diabetic group (n=15 per group). Animals were maintained under controlled temperature (25°C) and lighting (14/10 light/dark cycle), and were allowed to have free access...

show abstract

“…Unlike VEGF, PlGF binds selectively to VEGFR-1 and thus its ability to activate tyrosine phosphorylation of VEGFR-2 is limited (VEGFR-1 may still elicit its role in angiogenesis by heterodimerization with VEGFR-2 and VEGFR-3) (Rahimi et al, 2000;Autiero et al, 2003;Dixelius et al, 2003). PlGF apparently does not lead to increased angiogenesis in response to hypoxia (Clauss et al, 1996;Cao et al, 1997;Shibuya et al, 1999;Simpson et al, 1999). In a study by Shih and co-workers, using the mouse model of OIR, intravitreal administration of PlGF prior to hyperoxic exposure protected the retinal vessels from hyperoxia-induced vasoattenuation without increasing neovascularization (Shih et al, 2003).…”

Section: Implications For Prevention and Treatment Of Ropmentioning

confidence: 99%

Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

636

527

View full text Add to dashboard Cite

Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis.

show abstract

Placenta Growth Factor: Identification and Characterization of a Novel Isoform Generated by RNA Alternative Splicing

Cited by 168 publications

References 27 publications

Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Streptozotocin-Induced Diabetes Decreases Placenta Growth Factor (PIGF) Levels in Rat Placenta

Vascular endothelial growth factor in eye disease

Contact Info

Product

Resources

About