Fetal Vasculogenesis and Angiogenesis in Human Placental Villi

Demir, Ramazan; Kaufmann, Peter; Castellucci, Mario; Erbengi, T.; Kotowski, A.

doi:10.1159/000146886

Cited by 241 publications

(53 citation statements)

References 11 publications

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“…Moreover, the placenta can produce the hematopoietic factor activin A (36), and levels of activin A are increased in PE (37). This factor may act locally; the murine (38,39) and human (40,41) placenta have been suggested to function as hematopoietic organs. Thus, increased hematopoietic activity in the preeclamptic placenta could explain the elevated levels of hemoglobin mRNA that we observed.…”

Section: Discussionmentioning

confidence: 99%

Placental expression profiling in preeclampsia: local overproduction of hemoglobin may drive pathological changes

Centlow

Carninci²,

Nemeth

et al. 2008

Fertility and Sterility

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Using microarrays made with cDNAs from subtracted placental libraries, we show increased hemoglobin production in the preeclamptic placenta. Heme and hemoglobin may cause endothelial damage and inflammation and drive pathological changes in the placenta if they are released there. Study Objective:To create a library enriched in cDNAs from preeclamptic placentas to print on to microarrays for placental profiling of preeclampsia (PE) and high risk pregnancies. Design: Prospective study.Setting: University women's clinic and academic research laboratory.Patients: Ten patients with PE, 5 with PE and bilateral notching, 5 with bilateral notching without PE, and 15 normotensive patients were recruited.Interventions: Placenta and placenta bed biopsies were collected after delivery. Main Outcome Measures:Subtracted libraries of PE transcripts were produced, and cDNAs from these libraries were used to make PE-specific cDNA arrays. Results were verified quantitatively using real-time PCR and histologically using in situ hybridization and immunohistochemistry.Results: 30 genes were significantly altered in at least one group comparison. Differences in two candidate genes were confirmed using quantitative rt-PCR. Hemoglobin α2 and γ transcripts were significantly over-expressed in the PE placenta. Scattered cells in the placenta and placental blood vessels were shown to express genes encoding these hemoglobin-chains. Conclusions:We demonstrate increased hemoglobin production in the PE placenta. The hemoglobin may be released into the placenta blood vessel lumen. Free heme and hemoglobin are potent toxins which cause endothelial damage and inflammation.

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Section: Discussionmentioning

confidence: 99%

Placental expression profiling in preeclampsia: local overproduction of hemoglobin may drive pathological changes

Centlow

Carninci²,

Nemeth

et al. 2008

Fertility and Sterility

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“…Angiogenesis and vascular transformation are important processes for normal development of the placenta and fetus [10]. 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].…”

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

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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...

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“…Vasculogenesis is evident early in placental development when cells within the fetal villi differentiate into fetal endothelial cells and are organised into functional vessels. Angiogenesis, the sprouting of new capillaries from existing vessels, is also an essential component of placental development (Demir et al 1989). Within the villi of the placenta the fetal vasculature must develop in such a way as to ensure that sufficient capacity for exchange occurs between fetal and maternal circulations.…”

Section: Introductionmentioning

confidence: 99%

Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

Clark

Smith²,

Licence³

et al. 1998

Journal of Endocrinology

192

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Fetal Vasculogenesis and Angiogenesis in Human Placental Villi

Cited by 241 publications

References 11 publications

Placental expression profiling in preeclampsia: local overproduction of hemoglobin may drive pathological changes

Placental expression profiling in preeclampsia: local overproduction of hemoglobin may drive pathological changes

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

Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

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