Structure, Expression and Receptor-Binding Properties of Placenta Growth Factor (PlGF)

Persico, M. Graziella; Vincenti, V.; DiPalma, T.

doi:10.1007/978-3-642-59953-8_2

Cited by 123 publications

(95 citation statements)

References 23 publications

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“…Indeed, transcripts encoding mouse PlGF were abundant in trophoblastic giant cells associated with the parietal yolk sac at early stages of embryogenesis suggesting a role to coordinate vascularization in the deciduum and placenta during early embryogenesis (Achen et al, 1997). In addition PlGF is expressed at a low level in several other organs including the heart, lung, thyroid, skeletal muscle, and adipose tissue under normal physiological conditions (Viglietto et al, 1995;Persico et al, 1999;Voros et al, 2005).…”

Section: Plgf Expressionmentioning

confidence: 99%

The discovery of placenta growth factor and its biological activity

2012

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Abbreviations: BF-2, forkhead/winged helix transcription factor FoxD1; eNos, enodothelial nitric oxide synthase; HIFs, hypoxia inducible factors; HRE, hypoxia responsive element; MTF-1, metal transcription factor 1; NRP1 and NRP2, neuropilin 1 and 2; PlGF, placenta growth factor; TACE, TNF-α converting enzyme; TAM, tumor-associated macrophages; TIMP-3, tissue inhibitor of metalloproteinases; TK, tyrosine kinase; VEGFR-1 and VEGFR-2, VEGF receptor 1 and 2 AbstractAngiogenesis is a complex biological phenomenon crucial for a correct embryonic development and for post-natal growth. In adult life, it is a tightly regulated process confined to the uterus and ovary during the different phases of the menstrual cycle and to the heart and skeletal muscles after prolonged and sustained physical exercise. Conversly, angiogenesis is one of the major pathological changes associated with several complex diseases like cancer, atherosclerosis, arthritis, diabetic retinopathy and age-related macular degeneration. Among the several molecular players involved in angiogenesis, some members of VEGF family, VEGF-A, VEGF-B and placenta growth factor (PlGF), and the related receptors VEGF receptor 1 (VEGFR-1, also known as Flt-1) and VEGF receptor 2 (VEGFR-2, also known as Flk-1 in mice and KDR in human) have a decisive role. In this review, we describe the discovery and molecular characteristics of PlGF, and discuss the biological role of this growth factor in physiological and pathological conditions.

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Section: Plgf Expressionmentioning

confidence: 99%

The discovery of placenta growth factor and its biological activity

2012

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“…KDR mediates the major growth and permeability actions of VEGF, whereas Flt1 may have a negative role, either by acting as a decoy receptor or by suppressing signaling through KDR. Placental growth factor (PlGF) was the first VEGF relative identified to be abundantly expressed in the placenta and it acts by binding to Flt1 but not KDR (Persico et al, 1999). VEGF-C and VEGF-D, based on their ability to bind the lymphatic-specific Flt3 receptor (also known as VEGFR3), seem to be important for lymphatic development (Jussila and Alitalo, 2002;Olofsson et al, 1999).…”

Section: Angiogenic Factors In the Pathogenesis Of Preeclampsiamentioning

confidence: 99%

Angiogenic factors and natural killer (NK) cells in the pathogenesis of preeclampsia

Kopcow

Karumanchi

2007

Journal of Reproductive Immunology

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Preeclampsia is a pregnancy-specific complex disease in which numerous genetic, immunological and environmental factors interact. Characterized by new onset hypertension, proteinuria and edema after 20 weeks of gestation, preeclampsia is often complicated by small-for-gestational-age (SGA) babies and preterm delivery, and is therefore a significant cause of maternal and fetal morbidity and mortality. The only definitive treatment of preeclampsia is delivery of the placenta. Recent data suggest that the anti-angiogenic state induced by excess circulating anti-angiogenic factors of placental origin may be responsible for the clinical signs and symptoms of preeclampsia. Natural killer (NK) cells at the maternal/fetal interface, which are thought to play an important role in normal placental development, have been noted recently to induce angiogenic factors and vascular remodeling. Moreover, genetic studies suggest that susceptibility to preeclampsia may be influenced by polymorphic HLA-C ligands and killer cell receptors (KIR) present on NK cells. This review summarizes our current understanding of the role of angiogenic factors and NK cells in the pathogenesis of preeclampsia.

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“…FLT1) and VEGFR-2 (fetal liver kinase, Flk1/ KDR), PlGF binds only to FLT1 and sFLT1, the natural soluble version of the receptor lacking transmembrane and intracellular domains (Kendall and Thomas 1993). PlGF-2 can also bind to neuropilin (NRP)-1 and -2 because of an insertion of 21 basic amino acids at the carboxyl terminus (Migdal et al 1998;Persico et al 1999). PlGF-1 and PlGF-3 are diffusible isoforms, whereas PlGF-2 and PlGF-4 have heparin binding domains (Yang et al 2003).…”

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confidence: 99%