Developmental expression and regulation of basic fibroblast growth factor and vascular endothelial growth factor in rat decidua and in a decidual cell line

Srivastava, R. K.; Gu, Yun; Ayloo, Swathi; Zilberstein, M.; Gibori, Geula

doi:10.1677/jme.0.0210355

Cited by 43 publications

(33 citation statements)

References 46 publications

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“…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].…”

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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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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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“…Multiplex reverse transcriptase-polymerase chain reaction. Primers for VEGF, KDR, Flt, and rat ribosomal phosphoprotein P0 (RRRPP0) were designed as previously described (61). Forward primers were 5Ј-GGA-CCC-TGA-CTT-TAC-TGC-TGT-ACC-3Ј, 5Ј-TGG-CTC-ACA-GGC-AAC-ATC-3Ј, 5Ј-CTG-ACT-CTC-GGA-CCC-CTG-3Ј, and 5Ј-TCT-CCC-CCT-TCT-CCT-TCG-3Ј for VEGF, KDR, Flt, and RRRPP0, respectively.…”

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confidence: 99%

Cyclic Stretch and Hypertension Induce Retinal Expression of Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor—2

et al. 2001

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A single exposure to 20% symmetric static stretch increased KDR mRNA expression 3.9 ± 1.1-fold after 3 h (P = 0.002), with a gradual return to baseline within 9 h. In contrast, BRECs exposed to cardiac-profile cyclic stretch at 60 cpm continuously accumulated KDR mRNA in a transcriptionally mediated, time-dependent and stretchmagnitude-dependent manner. Exposure to 9% cyclic stretch increased KDR mRNA expression 8.7 ± 2.9-fold (P = 0.011) after 9 h and KDR protein concentration 1.8 ± 0.3-fold (P = 0.005) after 12 h. Stretched-induced VEGF responses were similar. Scatchard binding analysis demonstrated a 180 ± 40% (P = 0.032) increase in high-affinity VEGF receptor number with no change in affinity. Cyclic stretch increased basal thymidine uptake 60 ± 10% (P < 0.001) and VEGF-stimulated thymidine uptake by 2.6 ± 0.2-fold (P = 0.005). VEGFNAb reduced cyclic stretch-induced thymidine uptake by 65%. Stretched-induced KDR expression was not inhibited by AT1 receptor blockade using candesartan. Hypertension increased retinal KDR expression 67 ± 42% (P < 0.05) in SHR rats compared with normotensive WKY control animals. When hypertension was reduced using captopril or candesartan, retinal KDR expression returned to baseline levels. VEGF reacted similarly, but Flt expression did not change. These data suggest a novel molecular mechanism that would account for the exacerbation of diabetic retinopathy by concomitant hypertension, and may partially explain the principal clinical manifestations of hypertensive retinopathy itself. Furthermore, these data imply that anti-VEGF therapies may prove therapeutically effective for hypertensive retinopathy and/or ameliorating the deleterious effects of coexistent hypertension on VEGF-associated disorders such as diabetic retinopathy.

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“…Interestingly, when the temperature is shifted back to 33 8C, GG-AD cells dedifferentiate and regain features of the endometrial stromal cells. Several studies have already used this cell line to study the process of decidualization and observed similarities between this model and in vivo models of decidualization (10)(11)(12). Encouraged by these observations, we set out to examine the mechanism of apoptotic regression of decidual cells using the temperature-sensitive GG-AD cells as a model.…”

Section: Discussionmentioning

confidence: 97%

“…Furthermore, it has been shown that when GG-AD cells are maintained at 39 8C the expression of estrogen receptor b (ERb) (10), interleukin-6 (IL-6), IL-6 receptor and 130 kDa glycoprotein (gp130) (11), basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) (12) are increased. In the present study, we utilized the GG-AD cell line to assess directly the relationship between apoptotic regulators and decidualization.…”

Section: Introductionmentioning

confidence: 99%

The involvement of apoptotic regulators during in vitro decidualization

Akçalı

Gibori²,

Khan³

2003

European Journal of Endocrinology

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Objectives: The uterus responds to an implanting blastocyst by undergoing extensive tissue modification leading to decidualization. This modification includes differentiation and apoptosis of epithelial as well as stromal cell compartments. It is generally accepted that the decidual cell regression pattern is similar to the pattern of initial differentiation, suggesting that decidual cell death is the end point of timed differentiation. However, the molecular mechanisms controlling these events are not understood clearly. Therefore, we aimed to investigate the involvement of apoptotic factors using an in vitro cell culture system. Design: In order to assess the role of apoptotic factors during decidualization, we used a decidual cell line (GG-AD) that had been transformed with a temperature-sensitive SV-40 mutant. At the non-permissive temperature (39 8C), these cells showed the characteristics of differentiated decidual cells. They dedifferentiated into stromal cells when the temperature was shifted back to 33 8C. Methods: We performed Northern blot analysis for bax, bcl-x L and bcl-2 at both temperatures. The onset of apoptosis was examined by Annexin V staining. The expression of p53 protein was also determined by Western blot. Results: We found an increase in the expression of bax when GG-AD cells were grown at 39 8C. We also showed apoptosis with Annexin V staining at 39 8C. The p53 protein expression was also similar to that of the animal models, suggesting that the programmed cell death of the decidual cells occurred in a p53-independent manner. Conclusions: These data indicate that a parallelism exists between the increased expression of proapoptotic genes and decidual cell death, similar to animal models. Therefore, an in vitro model of GG-AD cells can be used to assess directly the relationship between apoptotic regulators and decidualization and could be used to study the mechanism of decidual cell regression.

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Developmental expression and regulation of basic fibroblast growth factor and vascular endothelial growth factor in rat decidua and in a decidual cell line

Cited by 43 publications

References 46 publications

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

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

Cyclic Stretch and Hypertension Induce Retinal Expression of Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor—2

The involvement of apoptotic regulators during in vitro decidualization

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