Immunohistochemistry For Vascular Endothelial Growth Factor Research Articles

Vascular endothelial growth factor immunoexpression in oral paracoccidioidomycosis.

Paracoccidioidomycosis (PCM) is a systemic mycosis endemic and limited to Latin America. Brazil is responsible for more than 80% of diagnosed cases in the world. Since PCM is not a notifiable disease, there are still no accurate data on its incidence in Brazil. Vascular endothelial growth factor (VEGF) is considered the main vascular endothelial growth factor expressed in the process of angiogenesis, both under physiological and pathological conditions. To date, there are not studies in the literature that evaluated the expression of VEGF in oral PCM lesions. Therefore, the objective of this study was to evaluate the prevalence of oral lesions of PCM diagnosed from 1998 to 2020; to analyze the immunoexpression of VEGF in oral lesions of PCM; and to compare the VEGF immunostaining with the clinical and microscopic aspects of these lesions. Clinical data of 98 cases of patients with oral PCM were evaluated. A total of 41 selected cases were quantitatively and qualitatively analysed by immunohistochemistry for VEGF. Our results showed that oral PCM preferentially affects white males, with mean age of 50.2 years, and the gingiva and the alveolar ridge. It was not possible to correlate VEGF immunoexpression with clinical and microscopic variables. Oral PCM is a relatively uncommon pathological condition and that, in our sample, the immunoexpression of VEGF was mild and observed in a reduced number of cases.

Clinicopathologic significance of the delta-like ligand 4, vascular endothelial growth factor, and hypoxia-inducible factor-2α in gallbladder cancer.

Gallbladder cancer (GBC) is usually detected in advanced stages with a low 5-year survival rate. Delta-like ligand 4 (DLL4), vascular endothelial growth factor (VEGF), and hypoxia-inducible factor-2alpha (HIF2α) have been studied for their role in tumorigenesis and potential for therapeutic target, and multiple clinical trials of the agents targeting them are ongoing. We investigated the expression of these markers in surgically resected GBC and tried to reveal their association with the clinicopathologic features, mutual correlation of their expression, and prognosis of the GBC patients by their expression. We constructed the tissue microarray blocks of 99 surgically resected GBC specimens and performed immunohistochemistry of DLL4, VEGF, and HIF2α. We used the quantitative digital image analysis to evaluate DLL4 and VEGF expression, while the expression of HIF2α was scored manually. The expression of VEGF and HIF2α showed a significant trend with tumor differentiation (p= .028 and p= .006, respectively). We found that the high DLL4 and VEGF expression were significantly correlated with lymph node metastasis (p= .047, both). The expression of VEGF and HIF2α were significantly correlated (p < .001). The GBC patients with low HIF2α expression showed shorter recurrence-free survival than those with high HIF2α expression. This study suggested the possibility of the usage of DLL4 and VEGF to predict the lymph node metastasis and the possibility of VEGF and HIF2α to predict the expression level mutually. Further studies may be needed to validate our study results and eventually accelerate the introduction of the targeted therapy in GBC.

Aflibercept suppresses ovarian hyperstimulation syndrome: an experimental study in rats.

In this study, we aimed to determine the impact of the antiangiogenic medications, namely, aflibercept and cabergoline in the prevention and treatment of ovarian hyperstimulation syndrome in a rat model. A total of 36 female Wistar rats were randomly allocated to one of the five groups, including disease-free and ovarian hyperstimulation syndrome controls: Group no OHSS (control, n=6) received saline only intraperitoneally (i.p.); group just OHSS (ovarian hyperstimulation syndrome only, n=6) received 10 IU pregnant mare serum gonadotropin and 30 IU human chorionic gonadotropin subcutaneously to produce ovarian hyperstimulation syndrome; group cabergoline+OHSS (cabergoline+ovarian hyperstimulation syndrome, n=8) received 100 μg/kg oral cabergoline; group aflibercept (12.5 mg/kg)+OHSS (aflibercept+ovarian hyperstimulation syndrome, n=8) received 12.5 mg/kg i.p. aflibercept; and group aflibercept (25 mg/kg)+OHSS (aflibercept+ovarian hyperstimulation syndrome, n=8) received 25 mg/kg i.p. aflibercept. The groups were compared for ovarian weight, immunohistochemical vascular endothelial growth factor expression, spectrophotometric vascular permeability evaluated with methylene blue solution in peritoneal lavage, and body weight growth. Vascular endothelial growth factor immunoexpression was substantially greater in the just OHSS group (22.00±10.20%) than in the aflibercept (12.5 mg/kg)+OHSS (7.87±6.13%) and aflibercept (25 mg/kg)+OHSS (5.63±4.53%) groups (p=0.008 and p=0.005, respectively). Post-hoc tests indicated that cabergoline, 12.5 mg/kg aflibercept, and 25 mg/kg aflibercept decreased vascular permeability compared to the untreated ovarian hyperstimulation syndrome group (p=0.003, p=0.003, and p=0.001, respectively). JOH group had the heaviest ovaries, whereas aflibercept (25 mg/kg)+OHSS group had the lightest. In terms of body weight gain, cabergoline+OHSS group was substantially greater than the aflibercept (12.5 mg/kg)+OHSS and aflibercept (25 mg/kg)+OHSS groups (p=0.006 and p=0.007, respectively). Aflibercept, an antiangiogenic medication, decreased ovarian hyperstimulation syndrome by lowering the vascular permeability and vascular endothelial growth factor expression.

Does Hypochlorous Acid Cause Ototoxicity? An Experimental Study.

Hypochlorous acid (HOCl) is a weak acid that ionizes in water. It is an effective antiseptic exhibiting low toxicity on living tissues. We aimed to investigate the ototoxic effects of HOCl on an animal model by using electrophysiological and histological methods. The study comprised 32 Sprague-Dawley rats, which were separated into four groups: control group (A), saline solution group (B), 70% isopropyl alcohol + 2% chlorhexidine group (C), and HOCl group (D). After recording the auditory brainstem response (ABR) for basal hearing thresholds (8, 16, 24, and 32 kHz), 0.03 ml of the aforementioned materials was injected intratympanically three times every 2 days in groups B, C, and D. ABR measurements were repeated on the 7th and 21st days. All animals were sacrificed, and temporal bones were prepared for examinations of cochlear histology and vascular endothelial growth factor immunohistochemistry. Basal hearing levels were normal across all frequencies and groups, with no statistical differentiation. On the 7th and 21st days after the ABR test, all other groups demonstrated a significant deterioration in hearing levels compared with group A. When the results from 7th and 21st days were compared within group D, a partial recovery was observed. In histopathology, groups C and D demonstrated moderate and severe cochlear degeneration, along with decreased immunoreactivity in the organ of Corti, stria vascularis, and spiral ligament. This is the first study to evaluate the safety of using HOCl in otology. Although HOCI is less ototoxic than the disinfectant used, it may have a toxic effect on cochlea.Level of Evidence: Animal Research.

Influence of genistein and diadizine on regularity of estrous cycle in cyclic female Wistar rat: interaction with estradiol receptors and vascular endothelial growth factor.

Isoflavones are estrogenic compounds that exist in soy, clover, and peanuts. They are selective estrogen receptor modulators. The study was planned to explain the interactions of isoflavones with estrogen receptors alpha (ERα), beta (ERβ), and vascular endothelial growth factor (VEGF) expressions in ovarian and uterine tissues during different stages of the estrous cycle of regular cyclic female Wistar rats. Thirty-two regular cyclic females were divided equally into control group: fed casein-based diet and isoflavones group: fed casein-based diet and gavaged 50 mg/kg/day soy isoflavones extract 40%. The regularity of estrus cycles was monitored. Final body weight (FBW), weight gain (BWG), and ovarian and uterine weights were estimated. Histopathology and immunohistochemistry for ERα, Erβ, and VEGF in ovarian and uterine tissues were performed. All females (100%, n = 16) in control group showed regularity in estrous cycle compared to 62.5% (n = 10) in isoflavones group. Estrus and diestrus phases revealed prolongation and shortening in isoflavones rats than control, respectively. Nonsignificant variation was noted in the duration of the whole cycle of both groups. FBW and BWG significantly decreased however, ovarian and uterine weights increased significantly in all estrous phases of isoflavones group than control. Histopathology demonstrated an increase in number of follicles/ovaries besides, hyperplasia and proliferation of luminal epithelium with hydropic degeneration in the isoflavones group. Also, uterine connective tissue stroma showed edema in the isoflavones group during all estrous phases. Immunostaining percentages of ERα, Erβ, and VEGF protein expression were significantly elevated in the isoflavones group during all estrous phases. Isoflavones induced irregularity of the estrous cycle that was encountered by increased and altered ERα, Erβ, and VEGF expressions in ovarian and uterine tissues.

Brain Activity after Intermittent Hypoxic Brain Condition in Rats.

Hypoxic brain injury is accompanied by a decrease in various functions. It is also known that obstructive sleep apnea (OSA) can cause hypoxic brain injury. This study aimed to produce a model of an intermittent hypoxic brain condition in rats and determine the activity of the brain according to the duration of hypoxic exposure. Forty male Sprague–Dawley rats were divided into four groups: the control group (n = 10), the 2 h per day hypoxia exposure group (n = 10), the 4 h per day hypoxia exposure group (n = 10), and the 8 h per day hypoxia exposure group (n = 10). All rats were exposed to a hypoxic chamber containing 10% oxygen for five days. Positron emission tomography–computed tomography (PET-CT) brain images were acquired using a preclinical PET-CT scanner to evaluate the activity of brain metabolism. All the rats were subjected to normal conditions. After five days, PET-CT was performed to evaluate the recovery of brain metabolism. Western blot analysis and immunohistochemistry were performed with vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The mean SUV was elevated in the 2 h per day and 4 h per day groups, and all brain regions showed increased metabolism except the amygdala on the left side, the auditory cortex on the right side, the frontal association cortex on the right side, the parietal association cortex on the right side, and the somatosensory cortex on the right side immediately after hypoxic exposure. However, there was no difference between 5 days rest after hypoxic exposure and control group. Western blot analysis revealed the most significant immunoreactivity for VEGF in the 2, 4, and 8 h per day groups compared with the control group and quantification of VEGF immunohistochemistry showed more expression in 2 and 4 h per day groups compared with the control group. However, there was no significant difference in immunoreactivity for BDNF among the groups. The duration of exposure to hypoxia may affect the activity of the brain due to angiogenesis after intermittent hypoxic brain conditions in rats.

INVESTIGATION OF SFLT-1 AND VEGF EXPRESSION IN NORMOTENSIVE AND PREECLAMPTIC PLACENTA. AN IMMUNOHISTOCHEMICAL STUDY

Objectives: The pathogenesis of preeclampsia is still not clear, but endothelial dysfunction believed to be one of the most encountered problems during placenta development in preeclamptic patients. Both vascular endothelial growth factor (VEGF) and its antagonist, soluble Fms-Like tyrosine kinase-1 (sFlt-1), have roles in vascular function. In this study, we have investigated immunohistochemical expression of VEGF and sFlt-1 in term placenta of normotensive and preeclampsia patients. Methods: Totally twenty term placentas were obtained from pregnant women of which 10 preeclampsia patient and 10 normotensive. Placentas were dissected and tissue samples were subjected to routine tissue processing protocol, then embedded in paraffin blocks. Serial sections were obtained from paraffin blocks and stained with H&amp;amp;E and PAS for routine histopathology. VEGF and sFlt-1 immunohistochemistry was performed to the sections. Results: When compared to control group, severe pathological changes were observed in preeclamptic placentas. Increase in number of syncytial knots and intervillous bridges, hemorrhage in interstitium, dilatation and congestion in villous capillaries, increase in fibrin accumulation in villus stroma, and increase in thickening of basement membrane were very clear. VEGF expression was significantly higher in normotensive placentas compared to preeclamptic. On the other hand, sFlt-1 expression was significantly increased in preeclamptic placentas. Conclusions: When the VEGF and sFlt-1 expression was considered, higher expression of sFlt-1 at preeclampsia, but decrease in VEGF expression, might be related to endothelial dysfunction in preeclampsia. Overall, this study demonstrates, imbalance between VEGF and sFlt-1 is one of the major reason of endothelial dysfunction in preeclamptic placenta.

İskemi/Reperfüzyon Hasarı Sonrası Sıçanların Over ve Uterusunda IL-1 ve VEGF Değişiklikleri

Objective:Ischemia/reperfusion injury causes parenchymal and endothelial cell damage as a result of inflammation. Vascular endothelial growth factor (VEGF) expressed in every kind of tissue in human body has important roles in migration, proliferation, endothelial cell permeability, angiogenesis and vasculogenesis. IL-1 is a one of the cytokine family members, and plays important roles in hematopoiesis, inflammatory reactions and immune system regulation. Furthermore, auto-inflammatory diseases are treated by IL-1 as therapeutic agent. The aim of this study is to observe changes of VEGF and IL-1 immunreactivity in ischemia/reperfused rat uterus and ovary.Method:Rats were separated into two groups. Control group and ischemia/reperfusion group which rats were subjected to 45 min ischemia/45 min reperfusion. Samples from uterus and ovary were fixed with 10% neutral formaldehyde and stained with H&E. VEGF and IL-1 immunohistochemistry was applied.Results:Histopathological results showed severe degeneration of endometrium in uterus and ovarian follicles in ischemia/reperfusion group. VEGF and IL-1 immunoreactivity increased in uteruses and ovaries of ischemia/reperfusion group when compared to control groupConclusionIn consequence, the present results suggest that VEGF and IL-1 may be potential detection marker for ischemia/reperfusion injured uterus and ovary. Moreover, VEGF and IL-1 might be in relation with each other to regenerate uterus and ovary.

Immunolocalization of VEGF/VEGFR system in human fetal vomeronasal organ during early development

The vomeronasal system (VNS) is an accessory olfactory structure present in most mammals adhibited to the detection of specific chemosignals implied in social and reproductive behavior. The VNS comprises the vomeronasal organ (VNO), vomeronasal nerve and accessory olfactory bulb. VNO is characterized by a neuroepithelium constituted by bipolar neurons and supporting and stem/progenitor cells. In humans, VNO is present during fetal life and is supposed to possess chemoreceptor activity and participate in gonadotropin-releasing hormone neuronal precursor migration toward the hypothalamus. Instead, the existence and functions of VNO in postnatal life is debated. Vascular endothelial growth factor (VEGF) and its receptors (VEGFRs) have been demonstrated to play fundamental roles in various neurogenic events. However, there are no data regarding the localization and possible function of VEGF/VEGFRs in human fetal VNO. Therefore, this study was conceived to investigate the expression of VEGF/VEGFRs in human VNO in an early developmental period (9–12 weeks of gestation), when this organ appears well structured. Coronal sections of maxillofacial specimens were subjected to peroxidase-based immunohistochemistry for VEGF, VEGFR-1 and VEGFR-2. Double immunofluorescence for VEGF, VEGFR-1 or VEGFR-2 and the neuronal marker protein gene product 9.5 (PGP 9.5) was also performed. VEGF expression was evident in the entire VNO epithelium, with particularly strong reactivity in the middle layer. Strongly VEGF-immunostained cells with aspect similar to bipolar neurons and/or their presumable precursors were detected in the middle and basal layers. Cells detaching from the basal epithelial layer and detached cell groups in the surrounding lamina propria showed moderate/strong VEGF expression. The strongest VEGFR-1 and VEGFR-2 expression was detected in the apical epithelial layer. Cells with aspect similar to bipolar neurons and/or their presumable precursors located in the middle and basal layers and the detaching/detached cells displayed a VEGFR-1 and VEGFR-2 reactivity similar to that of VEGF. The basal epithelial layer exhibited stronger staining for VEGFRs than for VEGF. Cells with morphology and VEGF/VEGFR expression similar to those of the detaching/detached cells were also detected in the middle and basal VNO epithelial layers. Double immunofluorescence using anti-PGP 9.5 antibodies demonstrated that most of the VEGF/VEGFR-immunoreactive cells were neuronal cells. Collectively, our findings suggest that during early fetal development the VEGF/VEGFR system might be involved in the presumptive VNO chemoreceptor activity and neuronal precursor migration.

Demonstration of myocardial infarction in decomposed myocardium with vascular endothelial growth factor immunohistochemistry: A tropical climate study

Demonstration of myocardial infarction in decomposed myocardium with vascular endothelial growth factor immunohistochemistry: A tropical climate study

VEGF may contribute to macrophage recruitment and M2 polarization in the decidua.

It is increasingly evident that cytokines and growth factors produced in the decidua play a pivotal role in the regulation of the local immune microenvironment and the establishment of pregnancy. One of the major growth factors produced in the decidua is vascular endothelial growth factor (VEGF), which acts not only on endothelial cells, but also on multiple other cell types, including macrophages. We sought to determine whether decidua-derived VEGF affects macrophage recruitment and polarization using human endometrial/decidual tissue samples, primary human endometrial stromal cells (ESCs), and the human monocyte cell line THP1. In situ hybridization was used for assessment of local VEGF expression and immunohistochemistry was used for identification and localization of CD68-positive endometrial macrophages. Macrophage migration in culture was assessed using a transwell migration assay, and the various M1/M2 phenotypic markers and VEGF expression were assessed using quantitative real-time PCR (qRT-PCR). We found dramatic increases in both VEGF levels and macrophage numbers in the decidua during early pregnancy compared to the secretory phase endometrium (non-pregnant), with a significant increase in M2 macrophage markers, suggesting that M2 is the predominant macrophage phenotype in the decidua. However, decidual samples from preeclamptic pregnancies showed a significant shift in macrophage phenotype markers, with upregulation of M1 and downregulation of M2 markers. In THP1 cultures, VEGF treatment significantly enhanced macrophage migration and induced M1 macrophages to shift to an M2 phenotype. Moreover, treatment with conditioned media from decidualized ESCs induced changes in macrophage migration and polarization similar to that of VEGF treatment. These effects were abrogated by the addition of a potent VEGF inhibitor. Together these results suggest that decidual VEGF plays a significant role in macrophage recruitment and M2 polarization, and that inhibition of VEGF signaling may contribute to the shift in macrophage polarity observed in different pregnancy disorders, including preeclampsia.

Effects of siRNA-mediated HIF-1α gene silencing on angiogenesis in osteosarcoma.

Objective:To explore angiogenesis in osteosarcoma under the condition of hypoxia-inducible factor (HIF)-1α gene silenced by small interference RNA (siRNA).Methods:The SaOS-2 osteosarcoma cells, transfected with the recombinant plasmid pSilencer2.1-HIF-1α or pSilencer2.1-SCR, were classified as HIF-1α/siRNA group or SCR/siRNA group, respectively. In which, vascular endothelial growth factor (VEGF) immunohistochemistry were performed. HIF-1α and VEGF protein contents were detected by western blot. Gene expressions of HIF-1α and VEGF were quantified by qPCR. Then the transfected SaOS-2 cells were inoculated in nude mice and transplantation tumor were checked via HE staining, VEGF and CD34 immunohistochemistry, and calculation of microvascular density (MVD).Results:In vitro, VEGF immunohistochemistry stains, HIF-1α and VEGF protein contents, and the relative expressions of HIF-1α mRNA and VEGF mRNA in HIF-1α/siRNA group were obviously reduced. In vivo, morphological observation illustrated that heteromorphism were not obvious in the cells of HIF-1α/siRNA group and vascular systems were sparse in its transplantation tumor tissue, and immunohistochemistry revealed that both VEGF and CD34 stains were significantly decreased in HIF-1α/siRNA group, and MVD in HIF-1α/siRNA group (7.3±1.1) were obviously less than that in SCR/siRNA group (17.2±3.2) (P<0.05).Conclusion:Angiogenesis in osteosarcoma can be inhibited by siRNA-mediated HIF-1α gene silencing, which is expected to provide a novel and attractive target of therapeutic strategies of osteosarcoma.

The effect of vascular endothelial growth factor-1 expression on survival of advanced colorectal cancer patients

ABSTRACTColorectal cancer is third leading cause of cancer mortality. About 60% of patients had already developed metastasis at the time of diagnosis. Vascular endothelial growth factor (VEGF) is crucial for the development of neovascularization and hence metastasis. This study aimed at investigating the relation between the expression of VEGF in biopsies from surgically dissected colon cancer and the survival of those patients. Biopsies were collected from 86 patients with advanced colon cancer and sections were stained by immunohistochemistry for VEGF. Patients received chemotherapy after the operation and were followed up for disease progression and survival. The clinical data were statistically analyzed with respect to the immunohistochemistry results. The survival of the patients was significantly longer in the patients for whom biopsies showed negative or weak expression of VEGF in comparison to those with moderate to high expression (p-value = 0.04). The expression of VEGF was more frequent in the patients who died as a consequence of the disease in comparison to the 10-year survivors. In conclusion, VEGF could be related to the survival of the patients with colorectal carcinoma and should be considered as a predictor of the prognosis.

Simvastatin ameliorates vascular endothelial growth factor overexpression in a rat model of diabetic retinopathy: a histological and immunohistochemical study

Background and objectivesDiabetic retinopathy (DR) is one of the main causes of vision loss. Treatment options during its early stages are not available. This study was designed to evaluate the potential protective effects of simvastatin on experimentally induced DR, with special emphasis on its possible modulatory effect on vascular endothelial growth factor (VEGF).Materials and methodsThirty adult male albino rats were divided equally into three groups: group І (the control group), group II (the diabetic group), and group III (diabetic/simvastatin-treated group). Diabetes was induced by intraperitoneal injection of streptozotocin at a dose of 50 mg/kg/rat in 20 adult male albino rats. Simvastatin was administered orally as 20 mg/kg/rat 48 h after streptozotocin injection. Blood glucose levels and body weight were measured. Retinal specimens were processed for hematoxylin and eosin staining and VEGF immunohistochemistry. Morphometric analysis included measurement of retinal thickness and area percentage of VEGF. All results were statistically analyzed using the Student t-test and analysis of variance test.ResultsThe untreated group showed histological features of DR and increased VEGF immunoreactivity compared with controls. The simvastatin-treated group showed improved features of DR and decreased VEGF immunoreactivity.ConclusionThese results suggest that simvastatin has protective effects against DR by eliminating VEGF overexpression and might be considered a promising therapeutic agent for it.

The Expression of Cyclin D1, VEGF, EZH2, and H3K27me3 in Atypical Teratoid/Rhabdoid Tumors of the CNS: A Possible Role in Targeted Therapy.

Atypical teratoid/rhabdoid tumor (AT/RT) is an uncommon malignancy with a dismal outcome, which responds poorly to multimodality therapies. Animal studies have revealed Cyclin D1 as a possible therapeutic target. The addition of vascular endothelial growth factor (VEGF) inhibitors to chemotherapeutic regimens has shown promising results in pediatric central nervous system tumors. Enhancer of Zeste homolog 2 (EZH2) overexpression has been implicated in various cancers, including medulloblastomas. H3K27me3 is a new marker for pediatric high-grade gliomas. However, their role in AT/RT has not been evaluated sufficiently. We retrieved cases of AT/RT, and reviewed their clinical data and histopathologic features. Immunohistochemistry for Cyclin D1, VEGF, EZH2, and H3K27me3 was performed. Follow-up was noted when available. Fourteen cases of AT/RT were identified (mean age, 3.4 y; range, 10 mo to 8 y). Cyclin D1 immunopositivity was noted in all cases [labeling index (LI): 5% to 98%; mean, 41.3%]. VEGF positivity was seen in 83.3% of the cases. All cases showed EZH2 overexpression (mean LI, 74.3%; range, 32% to 96%). Reduction of H3K27me3 expression was noted in 63% of the cases, with no correlation with EZH2 LI. Two patients died of postoperative complications. Of the rest, follow-up was available for 7 (range, 7 to 120 wk): 1 achieved clinical remission, whereas 6 developed progressive disease, including 3 deaths. Varying degrees of immunoreactivity to Cyclin D1, VEGF, and EZH2 were noted in the majority of the AT/RTs, and detection of these markers may be of value in the development of novel therapeutic agents and in determining which patients can benefit from them. AT/RTs show reduction in H3K27me3 expression, independent of EZH2 expression, indicating that their interaction requires further evaluation.

Uncoupling of Vascular Endothelial Growth Factor (VEGF) and Inducible Nitric Oxide Synthase (iNOS) in Gingival Tissue of Type 2 Diabetic Patients.

In this study, we investigate the relation between vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in periodontal disease of diabetic and non-diabetic individuals. We evaluated immunohistochemical VEGF and iNOS expressions in gingival biopsies from healthy individuals (no chronic periodontitis (CP)), patients with periodontitis alone (CP), patients with diabetes alone (DM) and diabetic patients with chronic periodontitis (DM + CP). We found a significant positive correlation between VEGF and iNOS expression in non-diabetic groups, but not in diabetic ones. Periodontal clinical parameters were not found to be significantly correlated with the inflammatory markers in no-CP, CP, and DM groups, whereas in DM + CP, positive and significant correlations were found between all the considered periodontal parameters and epithelial VEGF and endothelial iNOS. The uncoupling of VEGF and iNOS expression in diabetic individuals could allow a greater involvement of the markers in the inflammatory process of periodontitis.

The relationship between the expression of vascular endothelial growth factor and angiogenesis in glenohumeral of diabetic rats

Objective To explore the relationship between the expression of vascular endothelial growth factor(VEGF)and angiogenesis in glenohumeral of diabetic rats. Methods The 15 specific pathogen free (SPF)male SD rats that weighing between 240 and 260 gram were randomly divided into two groups,namely the model group(10)and the control group(5).After the success of modeling,the rates of both groups were sacrificed, take synovial tissues of rotator cuff from each group, stain and evaluate them.The expression of VEGF was determined by immunohistochemistry and Western blotting.The evalution of vascular density was measured by CD34 immunoreactivity. Results The hyperemia of synovial tissue from rotator cuff was observerd in model group, which showed strong immunoreactivity compared with the synovial tissue in control group, the immunohistochemistry of VEGF was++++(4),+++(4),++(2)compared with the control group++ (4),+(1)(P<0.05), the CD34 immunohistochemical staining showed that the average number of vessels per×400 field of vision in the model group and the control group were(34.1±15.9)and(9.4±4.5)respectively(P<0.05).It also shows that the expression of VEGF was more than the control group by Western blot. Conclusion VEGF is more expressed in the synovial tissue of rotator cuff in diabetic rats, which may play a role in pathological mechanisms and angiogenesis of diabetic rats frozen shoulder. Key words: Diabetes; Frozen shoulder; Synovial; Vascular endothelial growth factor; Angiogenesis

MRI feature of meningeal metastasis and correlation of peritumoral brain edema and VEGF expression

Objective To discuss the MRI feature of meningeal metastasis and correlation of peritumoral brain edema and vascular endothelial growth factor(VEGF) expression. Methods 48 patients with meningeal metastasis were observed with plain and enhanced 1.5T magnetic resonance imaging scans, surgical removal of the tumor tissues was measured with VEGF immunohistochemistry. Results The patients with MC showed three types MRI feature. The more vascular endothelial growth factor of the tumor tissues expressed, the more peritumoral brain edema(χ2= 33.34,P< 0.01). Conclusion MRI scanning is necessary for clinical diagnosis in MC. There are positive correlation between the expression of vascular endothelial growth factor of the tumor tissues and peritumoral brain edema(P< 0.01). Key words: Meningeal metastasis; Vascular endothelial growth factor; Peritumoral brain edema

Expression of vascular endothelial growth factor in oral squamous cell carcinoma.

ObjectivesThe goal of this study was to determine the correlation of clinicopathological factors and the up-regulation of vascular endothelial growth factor (VEGF) expression in oral squamous cell carcinoma.Materials and MethodsImmunohistochemical staining of VEGF and quantitative real-time polymerase chain reaction (RT-PCR) of VEGF mRNA were performed in 20 specimens from 20 patients with oral squamous cell carcinoma and another 20 specimens from 20 patients with carcinoma in situ as a controlled group.ResultsThe results were as follows: 1) In immunohistochemical study of poorly differentiated and invasive oral squamous cell carcinoma, high-level staining of VEGF was observed. Significant correlation was observed between immunohistochemical VEGF expression and histologic differentiation, tumor size of specimens (Pearson correlation analysis, significance r>0.6, P<0.05). 2) In VEGF quantitative RT-PCR analysis, progressive cancer showed more VEGF expression than carcinoma in situ. Paired-samples analysis determined the difference of VEGF mRNA expression level between cancer tissue and carcinoma in situ tissue, between T1 and T2-4 (Student's t-test, P<0.05).ConclusionThese findings suggest that up-regulation of VEGF may play a role in the angiogenesis and progression of oral squamous cell carcinoma.

Vascular endothelial growth factor-A and transforming growth factor-β1 expression in postmenopausal osteoporosis

Background Vascular endothelial growth factor (VEGF) plays an important role in bone angiogenesis, whereas transforming growth factor-β1 (TGF-β1) modulates bone differentiation, matrix formation, and cytokine expression. Aim of the work The aim of the study was to assess the immune expression of VEGF and TGF-β1 in cells lining the bone trabeculae among postmenopausal womεν in relation to bone histomorphometry and their association with osteoporosis. Patients and methods A total of 30 postmenopausal women were recruited for the study. Bone mineral density was measured using DEXA. On the basis of the results of the DEXA scan, they were divided as follows: group I comprised 14 (46.7%) women with normal bone mineral density; group II comprised five (16.7%) women with osteopenia; and group III comprised 11 (36.7%) women with osteoporosis. Iliac crest bone biopsy was taken from each of them. Histomorphometrical study was carried out using H&E stain to evaluate the trabecular microarchitecture in addition to immunohistochemistry for both VEGF and TGF-β1. Results Histomorphometric analysis was statistically and significantly different among the three groups. The area percentage of both TGF-β1 protein and VEGF expression in cells lining the bone trabeculae was statistically and significantly lower in the osteoporotic group compared with the other two groups. A statistically significant negative correlation was found between age and menopause duration and TGF-β1 only. A significant positive correlation was found between trabecular bone thickness and both VEGF (r=0.762, P=0.000) and TGF-β1 (r=0.785, P=0.000). Regression analysis showed only VEGF (t=2.537, P=0.018), and not TGF-β1 (t=0.326, P=0.747), to have independent association with trabecular bone thickness. Conclusion The results of the current study support that VEGF and TGF-β1 may contribute to the pathogenesis of postmenopausal osteoporosis. Further studies on the role of both TGF-β1 and VEGF in postmenopausal osteoporotic patients will be helpful to clarify the etiopathogenesis and treatment of postmenopausal osteoporosis.