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Placental Growth Factor (placental + growth_factor)
Selected AbstractsPlacental growth factor (PlGF) inhibition reduces choroidal neovascularization in a mouse model for age-related macular degenerationACTA OPHTHALMOLOGICA, Issue 2007S VAN DE VEIRE Purpose: To evaluate whether and through which mechanism PlGF blockage can inhibit choroidal neovascularization (CNV) in a mouse model of age-related macular degeneration (ARMD). Methods: CNV was induced in mice by placing 3 Argon laser burns on the choroid. In a first experiment we compared CNV formation between PlGF knock-out and wild type mice. Secondly, 144 wild-type mice were injected every 2 days with 5, 10, 20 or 40 mg/kg of either an anti-PlGF-antibody, an anti-VEGF receptor-2 (VEGFR2) antibody or an irrelevant control antibody. The CNV lesions were evaluated on histological cross-sections. The amount of endothelial cells, pericytes and inflammatory cells in the lesions were morphometrically analyzed after immunostaining for CD31, smooth muscle alpha-actin and F4/80 respectively. Results: CNV formation was significantly reduced in the PlGF knockout mice. The dose-response experiment showed that the 20 mg/kg dose of anti-PlGF significantly reduced the number of vessels in the lesions as compared to control antibody (p= 0.045), although less than a comparable dose of anti-VEGFR2 (p=0.027). Moreover, smooth muscle cell coverage was significantly increased in the anti-PlGF treated (p=0.04) and reduced in the anti-VEGFR2 treated mice (p=0.03) as compared to control mice. Finally, a significant reduction in number of inflammatory cells was observed in the lesions treated with anti-PlGF (p=0.017) but not in the anti-VEGFR2 treated mice (p=0.33). Conclusions: Anti-PlGF treatment inhibits CNV formation in a mouse model for ARMD. Both anti-PlGF and anti-VEGFR2 impair capillary growth, but in contrary to VEGFR2 blockage, anti-PlGF also reduces inflammation and promotes vessel maturation. [source] Role of vascular endothelial growth factor and angiopoietin systems in serum of Crohn's disease patientsINFLAMMATORY BOWEL DISEASES, Issue 1 2008Inés D. Pousa Abstract Background: The purposes of this study were to determine soluble angiogenic factors in Crohn's disease (CD) patients and to compare these factors according to the pathological behavior of the disease in order to establish a possible relationship with its evolution in patients with CD. Methods: Blood samples were collected from 70 patients with CD, grouped according to their phenotypic behavior, and from 30 healthy controls. Vascular endothelial growth factor (VEGF), placental growth factor (PlGF), angiopoietin 1 (Ang1), angiopoietin 2 (Ang2), and their cognate receptors [VEGFR1, VEGFR2, and angiopoietin receptor tyrosine kinase (Tie2)] were assayed by ELISA. Results: Circulating levels of VEGF, PlGF, VEGFR1, Ang2, and Tie2 were significantly higher in CD patients than in healthy controls (489 ± 271 versus 335 ± 118 pg/mL, P < 0.001; 31 ± 9 versus 23 ± 9 pg/mL, P < 0.001; 1.7 ± 0.4 versus 1.0 ± 0.3 ng/mL, P < 0.001; 4.8 ± 2.0 versus 3.9 ± 2.0 ng/mL, P < 0.05; and 36 ± 5 versus 22 ± 7 ng/mL, P < 0.001, respectively). Conversely, CD patients showed significantly lower serum levels of Ang1 than healthy controls (40 ± 12 versus 67 ± 22 ng/mL; P < 0.001). No differences between the groups were found in VEGFR2 serum level. The circulating levels of the angiogenic factors did not differ significantly when the CD patients were classified according to pathological phenotype. Conclusions: In comparison with healthy controls, CD patients were found to have an active angiogenic profile, as detected by significant alterations in levels of angiogenesis soluble markers. These patients did not differ in serum levels of angiogenic factors according to phenotypic disease behavior. (Inflamm Bowel Dis 2007) [source] Solid emulsion gel as a vehicle for delivery of polyunsaturated fatty acids: implications for tissue repair, dermal angiogenesis and wound healingJOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MEDICINE, Issue 7 2008Kirill I. Shingel Abstract The paper describes preparation and biological characterization of the solid hybrid biomaterial that was designed for cell-targeted lipid delivery in healing tissues. The material referred to as ,solid emulsion gel' combines a protein-stabilized lipid emulsion and a hydrogel structure in a single compartment. The potential of the omega-3 (n-3)-fatty acids rich solid emulsion gel for tissue repair applications was investigated at the macro-, micro-, molecular and gene expression levels, using human fibroblasts and endothelial cells and a porcine model of full-thickness wounds. Being non-cytotoxic in vitro and in vivo, the biomaterial was found to affect cell metabolism, modulate expression of certain genes, stimulate early angiogenesis and promote wound repair in vivo. The neovascular response in vivo was correlated with upregulated expression of the genes involved in lipid transport (e.g. adipophilin), anti-apoptosis (e.g. heat shock proteins, haem oxygenase 1) and angiogenesis (vascular endothelial growth factor, placental growth factor). Collectively, the results of this study provide first evidence that the angiogenic response provided by solid emulsion gel-mediated delivery of n-3 fatty acids is an alternative to the topical administration of exogenous growth factors or gene therapy, and can be advantageously used for the stimulation of tissue repair in complex wounds. Copyright © 2008 John Wiley & Sons, Ltd. [source] Up-regulation of proproliferative genes and the ligand/receptor pair placental growth factor and vascular endothelial growth factor receptor 1 in hepatitis C cirrhosisLIVER INTERNATIONAL, Issue 7 2007Xiao X. Huang Abstract Background/Aims: Cirrhosis can lead to hepatocellular carcinoma (HCC). Non-diseased liver and hepatitis C virus (HCV)-associated cirrhosis with or without HCC were compared. Method: Proliferation pathway genes, immune response genes and oncogenes were analysed by a quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and immunostaining. Results: Real-time RT-PCR showed up-regulation of genes in HCV cirrhosis including the proliferation-associated genes bone morphogenetic protein 3 (BMP3), placental growth factor 3 (PGF3), vascular endothelial growth factor receptor 1 (VEGFR1) and soluble VEGFR1, the oncogene FYN, and the immune response-associated genes toll-like receptor 9 (TLR9) and natural killer cell transcript 4 (NK4). Expressions of TLR2 and the oncogenes B-cell CLL/lymphoma 9 (BCL9) and PIM2 were decreased in HCV cirrhosis. In addition, PIM2 and TLR2 were increased in HCV cirrhosis with HCC compared with HCV cirrhosis. The ligand/receptor pair PGF and VEGFR1 was intensely expressed by the portal tract vascular endothelium. VEGFR1 was expressed in reactive biliary epithelial structures in fibrotic septum and in some stellate cells and macrophages. Conclusion: PGF and VEGFR1 may have an important role in the pathogenesis of the neovascular response in cirrhosis. [source] Maternal plasma soluble fms-like tyrosine kinase-1 and free vascular endothelial growth factor at 11 to 13 weeks of gestation in preeclampsiaPRENATAL DIAGNOSIS, Issue 3 2010Ranjit Akolekar Abstract Objective To investigate the maternal plasma concentration of soluble fms-like tyrosine kinase-1 (sFlt-1) and free vascular endothelial growth factor (free-VEGF) at 11 to 13 weeks of gestation in patients destined to develop preeclampsia (PE) and to examine whether any possible differences in maternal plasma levels are related to uterine artery pulsatility index (PI) and maternal serum placental growth factor (PlGF). Methods Plasma free-VEGF, plasma sFlt-1, serum PlGF and uterine artery PI were measured at 11 to 13 weeks in 90 cases that subsequently developed PE and in 180 unaffected controls. Results In the majority of cases of PE and controls the levels of free-VEGF were undetectable. In the pregnancies that developed PE, compared to unaffected controls, uterine artery PI was higher, serum PlGF was lower but there was no significant difference in levels of sFlt-1. Conclusion Measurement of free-VEGF and sFlt-1 in maternal blood at 11 to 13 weeks of gestation is not useful in the prediction of pregnancies destined to develop PE. Copyright © 2010 John Wiley & Sons, Ltd. [source] Early onset preeclampsia and second trimester serum markersPRENATAL DIAGNOSIS, Issue 12 2009Geralyn M. Lambert-Messerlian Abstract Objective To examine serum markers measured in the second trimester to identify women who subsequently develop preeclampsia. Methods Clinically defined preeclampsia was confirmed in 45 women who had provided a serum sample as part of Down syndrome screening. Preeclampsia was categorized as mild or severe, as well as early (<32 weeks) or late onset. Each case was matched with five controls based on gestational age and date of serum collection. Stored sera were retrieved and tested for inhibin A, soluble vascular endothelial growth factor receptor 1 (sVEGF R1), placental growth factor (PlGF), and endoglin. Results were converted to multiples of the median (MoM) and compared in case and control pregnancies. Univariate analysis was used to identify the strongest markers, which were then used in a multivariate model. Results Inhibin A, PlGF, and endoglin were consistently associated with preeclampsia, especially for early onset disease. A multivariate model using the three markers could identify 50% of the pregnancies with early onset preeclampsia with a 2% false positive rate. Conclusion The levels of inhibin A, PlGF, and endoglin in the second trimester can be combined using a predictive model to provide individualized risk estimates for early onset preeclampsia. Copyright © 2009 John Wiley & Sons, Ltd. [source] The relationship of the level of circulating antiangiogenic factors to the clinical manifestations of preeclampsiaPRENATAL DIAGNOSIS, Issue 5 2009Young Nam Kim Abstract Objective This study investigated whether the antiangiogenic factors' concentrations differ according to the clinical manifestations of preeclampsia. Methods This study included 62 preeclampsia and compared the soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), and placental growth factor (PlGF) concentrations among patients with different clinical manifestations of preeclampsia. We also compared the patients with preeclampsia to 62 controls matched by age, gestational age, and parity after 20 weeks of gestation. Results The sEng concentrations were significantly elevated in early-onset than in late-onset preeclampsia (105.4 ± 37.9 vs 66.3 ± 36.0 ng/mL, p = 0.0008). Moreover, the sEng levels were also higher in severe preeclampsia compared to mild (42.5 ± 31.0 vs 79.2 ± 38.6 ng/mL, p = 0.0013) and in the small for gestational age (SGA) group compared to the group without SGA (68.3 ± 39.3 vs 85.7 ± 38.2 ng/mL, p = 0.0273). The sFlt-1 levels, however, did not reveal significant difference according to the onset-time, severity, and presence of SGA. The antiangiogenic factors' concentrations were not related with the degree of hypertension or proteinuria. Conclusion Altered antiangiogenic factors might be involved in the pathogenesis of preeclampsia with synergistic, but different roles. Especially, sEng may be more related with early and severe preeclampsia. Copyright © 2009 John Wiley & Sons, Ltd. [source] Gene expression in chorionic villous samples at 11 weeks' gestation from women destined to develop preeclampsiaPRENATAL DIAGNOSIS, Issue 10 2008Antonio Farina Abstract Objective To evaluate the direct alterations in mRNA expression among chorionic villous samples from 11 weeks' pregnant women who would develop preeclampsia (PE) later in the pregnancy. Method Case-control study encompassing five women destined to develop PE [cases matched 1:5 for gestational age (GA) with 25 controls]. We quantified mRNA expression on tissue samples from chorionic villous sampling (CVS) of normal and PE patients. We then assessed mRNA expressions of vascular endothelial growth factor (VEGFA), VEGFA receptor 1 (Flt-1), endoglin (Eng), placental growth factor (PlGF), transforming growth factor-,1 (TGF-,1), heme oxygenase-1 (HO-1) and superoxide dismutase (SOD). Data were analyzed by nonparametric rank analysis. Results For all the mRNA species considered in this study, all the mean observed ranks in the PE group were significantly altered compared to the rank expectation among controls. mRNA for Eng and TGF-,1 were the markers with the highest degree of aberration in PE, in respect to controls. The results are consistent with those already reported for the corresponding circulating proteins. mRNA for HO-1 and SOD were instead associated with the lowest aberration. Conclusion It is assumed that the pathogenesis of PE is associated with pathophysiological alterations to trophoblasts in early gestation. Our study has directly proved that gene expressions relating to angiogenesis or oxidative stress are altered in the first trimester trophoblasts that go on to develop PE later. These results would put the basis for a possible screening method for PE by using residual CVS. Copyright © 2008 John Wiley & Sons, Ltd. [source] Physiological distribution of placental growth factor and soluble Flt-1 in early pregnancyPRENATAL DIAGNOSIS, Issue 3 2008George Makrydimas Abstract Objective To examine the distribution of placental growth factor (PlGF), vascular endothelial growth factor (VEGF) and soluble VEGF receptor-1 (sFlt-1) in maternal and embryonic fluid compartments in early pregnancy. Method The concentrations of PlGF, VEGF and sFlt-1 were measured in coelomic fluid and maternal serum from 16 singleton pregnancies at 7.0,9.3 weeks. In six cases, amniotic fluid was also examined. Results The median concentration of PlGF was 14.1 (range 8.9,27.6) pg/mL in maternal serum, 13.9 (range 9.5,31.4) pg/mL in coelomic fluid and 8.9 (range 3.9,15.3) pg/mL in amniotic fluid. The concentration of PlGF increased between 7.0 and 9.3 weeks in maternal serum (p = 0.001) and decreased in coelomic and amniotic fluid (p = 0.001). The median concentration of sFlt-1 was 8561 (range 6724-10 673) pg/mL in coelomic fluid, 523 (range 244,986) pg/mL in maternal serum, 30 (range 12,83) pg/mL in amniotic fluid (p = 0.0001), and it did not change significantly with gestation. VEGF was undetectable in most of the samples, and therefore, no further analysis was performed. Conclusion PlGF and sFlt-1 are present in the maternal and fetal fluid compartments in very early pregnancy, and their distribution is consistent with their site of production and the local conditions of transport. Copyright © 2008 John Wiley & Sons, Ltd. [source] PlGF expression in pre-invasive and invasive lesions of uterine cervix is associated with angiogenesis and lymphangiogenesisAPMIS, Issue 11 2009SHOUHUA YANG Most vascular endothelial growth factors (VEGF) have been shown to be associated with lymphangiogenesis and angiogenesis in various cancers. However, whether placental growth factor (PlGF), a rarely mentioned VEGF member, is involved in the pathogenesis of uterine cervical lesions remains unclear. To address this issue, we examined the relationship between PlGF expression and clinicopathologic variables in patients with pre-invasive and invasive lesions of uterine cervix. Sixty-two cervical specimens were immunostained with PlGF polyclonal antibody to define PlGF expression, and monoclonal antibodies D2-40 and CD34 to evaluate the lymphatic vessel density (LVD) and blood vessel density (BVD) of the lesions. PlGF mRNA level was detected by RT-PCR in all lesions from fresh tissues. We found that the levels of PlGF protein and mRNA expression were related to clinical stages (p < 0.05), but not to other clinicopathologic variables. No significant difference in PlGF expression was observed between squamous carcinoma and adenocarcinoma. Increased LVD and BVD were all associated with advanced stages (p < 0.001). Although LVD was strongly correlated with BVD, only high LVD was associated with pelvic lymphatic metastasis. Moreover, the level of PlGF expression was associated with both BVD(r = 0.715, p < 0.001) and LVD(r = 0.321, p < 0.05). Together, our study suggests that PlGF may participate in both tumor-associated angiogenesis and lymphangiogenesis of cervical carcinogenesis. [source] The interrelationship of complement-activation fragments and angiogenesis-related factors in early pregnancy and their association with pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 4 2010AM Lynch Please cite this paper as: Lynch A, Murphy J, Gibbs R, Levine R, Giclas P, Salmon J, Holers V. The interrelationship of complement-activation fragments and angiogenesis-related factors in early pregnancy and their association with pre-eclampsia. BJOG 2010; 117:456,462. Objective, To determine the interrelationships during early pregnancy of complement-activation fragments Bb, C3a and sC5b-9, and angiogenesis-related factors placental growth factor (PiGF), soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), and their associations with pre-eclampsia. Design, Prospective cohort study. Setting, Denver complement study (June 2005,June 2008). Population, A total of 668 pregnant women with singleton gestations, recruited between 10 and 15 weeks of gestation. Methods, Using univariable and multivariable logistic regression analysis, concentrations of complement-activation fragments and angiogenesis-related factors were compared between 10 and 15 weeks of gestation in women who subsequently did or did not develop pre-eclampsia. Interrelationships between these variables were tested using the non-parametric Spearman rank correlation coefficient. Main outcome measure, Pre-eclampsia. The association of complement-activation fragments and angiogenesis-related factors with obesity was also examined. Results, The mean (±SD) levels of complement Bb in early pregnancy among women who did and did not develop pre-eclampsia were 0.84 (±0.26) ,g/ml and 0.69 (±0.2) ,g/ml, respectively (P = 0.001). Concentrations of PiGF were significantly (P = 0.01) lower (31 ± 12 pg/ml) in early pregnancy in the pre-eclamptic group of women, as compared with the normotensive group (39 ± 32 pg/ml). The adjusted odds ratio (AOR) of Bb and PiGF were 2.1 (CI = 1.4,3.1, P < 0.0003) and 0.2 (CI = 0.07,0.7, P = 0.01), respectively. There was no significant difference in the levels of C3a, sC5b-9, sFlt-1 and sEng in early pregnancy among women who developed pre-eclampsia, compared with women who remained normotensive during pregnancy. Higher levels of Bb (P = 0.0001) and C3a (P = 0.03), and lower levels of sFlt-1 (P = 0.0002) and sEng (P = 0.0001) were found among women with obesity, compared with non-obese controls. No meaningful relationships were found between the complement-activation fragments and the angiogenesis-related factors. Conclusions, In this cohort during early pregnancy, increased concentrations of complement-activation factor Bb and lower concentrations of PiGF were associated with the development of pre-eclampsia later in pregnancy. [source] Different profiles of circulating angiogenic factors and adipocytokines between early- and late-onset pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 3 2010H Masuyama Please cite this paper as: Masuyama H, Segawa T, Sumida Y, Masumoto A, Inoue S, Akahori Y, Hiramatsu Y. Different profiles of circulating angiogenic factors and adipocytokines between early- and late-onset pre-eclampsia. BJOG 2010;117:314,320. Objective, Circulating angiogenic factors have been shown to be important in the pathophysiology of pre-eclampsia. Blood levels of adipocytokines differ in pre-eclampsia relative to controls and may also play an important role in disease pathogenesis. Differences in the circulating levels of these molecules were compared between matched normotensive controls and women with pre-eclampsia with onset before or at/after 32 weeks, and according to whether the women were of normal weight (18.5 < body mass index < 25) or overweight. Design, A cross-sectional study of 110 pregnant Japanese women who visited the Department of Obstetrics and Gynecology, Okayama University Hospital, Okayama, Japan. Setting, Tertiary referral centre serving 2000 births. Methods, Serum concentrations of soluble fms-like tyrosine kinase 1 (sFlt-1), placental growth factor (PlGF), soluble endoglin (sEng), adiponectin and leptin were measured in women with pre-eclampsia and in normotensive controls matched for age, gestational week, parity and body mass index. Main outcome measures, Serum levels of sFlt-1, PlGF, the sFlt-1/PlGF ratio, sEng, adiponectin and leptin. Results, The sFlt-1/PlGF ratio in early-onset pre-eclampsia was significantly higher than that in late-onset pre-eclampsia (112.0 ± 30.2 versus 45.4 ± 43.8, P = 0.037). There was a significant elevation of leptin in both subtypes relative to controls (early: 58.6 ± 18.3 ng/ml versus 26.0 ± 6.7 ng/ml, P = 0.001; late: 39.5 ± 9.2 ng/ml versus 22.0 ± 4.3 ng/ml, P = 0.005), but adiponectin was increased only in late-onset pre-eclampsia (36.5 ± 13.4 ,g/ml versus 12.0 ± 4.3 ,g/ml, P = 0.003). Significant differences in angiogenic factors and adiponectin were found between normal and overweight women only in late-onset pre-eclampsia. Conclusions, These data suggest that there are different profiles of angiogenic factors and adipocytokines between women who develop early- and late-onset pre-eclampsia. [source] First trimester urinary placental growth factor and development of pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 5 2009MD Savvidou Objective, To compare urinary placental growth factor (PlGF) concentration at 11+0 to 13+6 weeks of gestation in women who subsequently develop pre-eclampsia with normotensive controls. Design, Nested case,control study within a prospective study for first trimester prediction of pre-eclampsia. Setting, Routine antenatal visit in a teaching hospital. Population, Fifty-two women who developed pre-eclampsia and 52 controls matched for gestational age and sample storage time. Methods, Urinary PlGF concentration and PlGF to creatinine ratio were measured in women who developed pre-eclampsia and their matched controls. Comparisons between groups were performed using Student's t test. Main outcome measures, Development of pre-eclampsia. Results, In the pre-eclampsia group, the median urinary PlGF concentration (20.6 pg/ml, interquartile range [IQR] 9.1,32.0 pg/ml) and median urinary PlGF to creatinine ratio (1.6 pg/mg, IQR 1.2,2.5 pg/mg) were not significantly different from the control group (11.8 pg/ml, IQR 5.5,29.8 pg/ml, P = 0.1 and 1.7 pg/mg, IQR 1.2,2.3 pg/mg, P = 0.3, respectively). There were no significant differences between women with early-onset pre-eclampsia requiring delivery before 34 weeks (n = 13) and those with late-onset pre-eclampsia (n = 39) and between women with pre-eclampsia and fetal growth restriction (FGR) (n = 25) and those with pre-eclampsia and no FGR (n = 27) in either median PlGF concentration or median urinary PlGF to creatinine ratio. Conclusions, The development of pre-eclampsia is not preceded by altered urinary PlGF concentration in the first trimester of pregnancy. [source] 2164: Role of placental growth factor (PIGF) in wound healing after glaucoma filtration surgeryACTA OPHTHALMOLOGICA, Issue 2010T VAN BERGENArticle first published online: 23 SEP 2010 Purpose Failing filtering surgery due to excessive wound healing is a considerable challenge in ophthalmology, and largely contributes to progressive vision loss in glaucoma patients. Anti-VEGF therapy helps to prevent post-surgical scarring by inhibiting angiogenesis and collagen deposition, but does not influence inflammation (which is also an important player in postoperative wound healing). We will check the hypothesis that placental growth factor (PlGF) plays a role in scar formation after glaucoma filtration surgery, and that it may be a(n) (additional) target for improvement of the outcome of this surgery through its known anti-angiogenic and anti-inflammatory, and possibly anti-fibrotic properties. Methods The effect of an anti-PlGF antibody (ThromboGenics) will be investigated in vitro on the proliferation of endothelial cells (HUVEC), inflammatory cells (Jurkat cells) and of Tenon fibroblasts (TF). The effect of the antibody will also be investigated in vivo in a rabbit model for glaucoma surgery by measuring intra-ocular pressure (IOP), filtration bleb function and survival, and by (immuno-)histological analysis of angiogenesis (CD31), inflammation (CD45) and fibrosis (Sirius Red). Conclusion Our proposed research project will elucidate the potential role of PlGF-inhibition in the improvement of filtration surgery outcome, and will highlight any angiostatic, anti-inflammatory, and/or anti-fibrotic effects. PlGF-inhibition as an adjuvant anti-inflammatory therapy to anti-VEGF treatment in glaucoma surgery might open new perspectives for more efficient surgery. In conclusion, our project opens exciting perspectives for the treatment of the blinding condition of glaucoma, and thus might improve the visual prognosis of glaucoma patients. [source] Differential mitogenic responses of human macrovascular and microvascular endothelial cells to cytokines underline their phenotypic heterogeneityCELL PROLIFERATION, Issue 3 2001I. Lang A variety of growth factors promote the complex multistep process of angiogenesis. The mitogenic activity of vascular endothelial growth factors (VEGFs) and placental growth factors (PlGFs), known as cytokines acting predominantly on endothelial cells, was tested on human umbilical vein endothelial cells (HUVEC) and microvascular endothelial cells (MIEC) and compared with the potency of the universally acting basic fibroblast growth factor (FGF-2). The cells were seeded at different cell numbers and incubated with various doses of growth factors for a period of 24,72 h in culture medium ± serum. Proliferation was determined by measuring the optical density after staining the cells with the tetrazolium salt WST-1. VEGF121 and VEGF165 increased the number of HUVEC and MIEC at low and high seeding densities various doses and incubation times. The efficiency of FGF-2 was less pronounced at high seeding densities of the cells under serum-free conditions. PlGF-1 and PlGF-2 stimulated mitogenesis on HUVEC only at low cell numbers and after a short incubation time by 125 ± 3% and 102 ± 5% (P < 0.001), respectively. Longer incubation times with the lower seeding density in the absence of FCS did not induce a significant stimulatory effect of the PlGFs. MIEC responded stronger to all growth factors. In particular under serum free conditions, PlGF-1 and PlGF-2 effectively stimulated cell proliferation by 247 ± 54% (P < 0.01) and 288 ± 40% (P < 0.05) at low cell numbers, and by 81 ± 13% (P < 0.05) and 49 ± 13% (P < 0.01), respectively, at high cell numbers. The addition of fetal calf serum caused a reduced proliferative response of all growth factors on both cell types related to the controls. In conclusion, MIEC and HUVEC differ in their proliferative response to VEGFs, PlGFs and FGF-2. [source] | |||||||||||||