Wyniki wyszukiwania

1

Role of vascular endothelial growth factor in ovarian physiology - an overview

100%

Kaczmarek M. M., Schams D., Ziecik A. J.

Reproductive Biology

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2005

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tom 05

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nr 2

2

Vascular endothelial growth factor in systemic lupus erythematosus: relationship to disease activity, systemic organ manifestation, and nailfold capillaroscopic abnormalities

88%

Kuryliszyn-Moskal A., Klimiuk P. A., Sierakowski S., Ciolkiewicz M.

Archivum Immunologiae et Therapiae Experimentalis

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2007

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tom 55

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nr 3

3

Density of intranodal lymphatics and VEGF-C expression in B-cell lymphoma and reactive lymph nodes

88%

Wrobel T., Mazur G., Dziegiel P., Jelen M., Szuba A., Kuliczkowski K., Zabel M.

Folia Histochemica et Cytobiologica

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2006

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tom 44

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nr 1

4

Expression of vascular endothelial growth factor [VEGF] and its receptor FLK-1 in non-small cell lung cancer [NSCLC] - a preliminary report

88%

Dziadziuszko R., Chyczewski L., Jassem E., Jassem J.

Folia Histochemica et Cytobiologica. Supplement

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2001

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tom 39

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nr 1

5

Placental vascular endothelial growth factor expression in pregnancies complicated by type 1 diabetes

75%

Iciek R., Wender-Ozegowska E., Mikolajczak P., Seremak-Mrozikiewicz A., Zawiejska A., Mrozikiewicz P. M., Drews K., Brazert J.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 4

6

Growth factors and their receptors derived from human amniotic cells in vitro

75%

Grzywocz Z., Pius-Sadowska E., Klos P., Gryzik M., Wasilewska D., Aleksandrowicz B., Dworczynska M., Sabalinska M., Hoser G., Machalinski B., Kawiak J.

Folia Histochemica et Cytobiologica

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2014

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tom 52

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nr 3

7

Manipulation of ovarian follicle development by injecting vascular endothelial growth factor (VEGF) gene

75%

Shimizu T., Sato E.

Reproductive Biology

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2005

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tom 05

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nr 3

8

Biological properties of human skeletal myoblasts genetically modified to simultaneously overexpress the pro-angiogenic factors vascular endothelial growth factor-A and fibroblast growth factor-4

75%

Zimna A., Janeczek A., Rozwadowska N., Fraczek M., Kucharzewska P., Rucinski M., Mietkiewski T., Kurpisz M.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 2

9

High levels of soluble vascular endothelial growth factor receptor 1/sFlt1 and low levels of vascular endothelial growth factor in follicular fluid on the day of oocyte retrieval correlate with ovarian hyperstimulation syndrome regardless of the stimulation protocol

75%

Jakimiuk A. J., Nowicka M. A., Zagozda M., Koziol K., Lewandowski P., Issat T.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 3

10

Antitumor effects of recombinant antivascular protein ABRaA-VEGF121 combined with IL-12 gene therapy

75%

Ciomber A., Smagur A., Mitrus I., Cichon T., Smolarczyk R., Sochanik A., Szala S., Jarosz M.

Archivum Immunologiae et Therapiae Experimentalis

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2014

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tom 62

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nr 2

11

Antiangiogenic potential of grape stem extract through inhibition of vascular endothelial growth factor expression

75%

Stagos D., Apostolou A., Poulios E., Kermeliotou E., Mpatzilioti A., Kreatsouli K., Koulocheri S. D., Haroutounian S. A., Kouretas D.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

12

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Identification of potential off-targets of chemotherapeutic agent Sorafenib: a molecular docking approach

75%

Sahrawat T. R., Chawla P.

International Letters of Natural Sciences

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2016

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tom 51

B-Raf is a multi- drug target serine/threonine protein kinase, involved in the transduction of mitogenic signals from the cell membrane to the nucleus. Mutated B-Raf causes overactive downstream signaling via MEK and ERK, leading to excessive cell proliferation and survival, independent of growth factors causing cancers such as Pancreatic carcinoma. A novel bi-aryl urea- Sorafenib, is a potent inhibitor of Raf-1 that has been approved for the treatment of a number of cancers including pancreatic cancer. The present investigation was designed to identify the potential off-targets of Sorafenib which could be responsible for its reported undesirable side effects. Molecular docking was used to test the efficacy of structural analogs of Sorafenib against B-Raf using FlexX and it was found that the analog with CID:10151557 had a high potency with minimum number of clashes, low lipophilic score and high match score, similar to Sorafenib. To identify the potential off-target/s of Sorafenib, macromolecular surface similarity detection software MEDIT SA MED-SuMo was used and the results obtained were validated through literature. The possible off-targets obtained belonged to the family of protein tyrosine kinases i.e. VEGFR-2, VEGFR-3, platelet-derived growth factor receptor beta, Flt-3, and c-KIT, each of which were docked with Sorafenib. Based on high docking scores and similarity with B-Raf for its binding site interacting residues, it was concluded that Vascular endothelial growth factor tyrosine kinase receptor (VEGFR) is a potential off-target of anti-cancer chemotherapeutic agent Sorafenib.

13

Post-transcriptional modifications of VEGF-A mRNA in non-ischemic dilated cardiomyopathy

75%

Kowalczyk J., Domal-Kwiatkowska D., Mazurek U., Zembala M., Michalski B., Zembala M.

Cellular and Molecular Biology Letters

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2007

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tom 12

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nr 3

Vascular endothelial growth factor (VEGF-A) is one of the most important proangiogenic factors. It has many isoforms encoded by one gene. The occurrence of these isoforms is associated with the process of alternative splicing of mRNA. Some of the splice forms are perceived as tissue specific. The aim of this study was to determine the alternative splicing of VEGF-A mRNA in dilated cardiomyopathy, especially at the level of particular myocardial layers. The assessment of post-transcriptional modifications of VEGF-A mRNA was made on specimens taken from the explanted hearts of patients undergoing cardiac transplantation. Molecular and histopathological studies were perfomed on particular layers of the myocardial muscle (endocardium, myocardium, epicardium). A molecular analysis of cardiac samples was performed by quantitative analysis of the mRNA of the studied VEGF-A isoforms (VEGF121, -145, -165, -183, -189, and -206) using QRTPCR with an ABI-PRISM 7700-TaqMan sequence detector. 72 cardiac specimens taken from the explanted hearts were analyzed. Each of the studied VEGF-A splice forms was present in the evaluated hearts, but the types of alternative splicing of mRNA were different in particular layers. Quantitative analysis revealed different amounts of the studied isoforms. Generally, significantly increased expression of the VEGF-A isoforms was observed in samples taken from hearts with post-inflammatory etiology of cardiomyopathy. Our conclusions are: 1. All the studied VEGF-A isoforms were found in the human hearts, including those thusfar considered characteristic for other tissues. 2. Significant differences were observed in the expression of the VEGF-A splice forms with respect to the myocardial layers and the location of the cardiac biopsy. 3. Repetitive and comparable results for samples with post-inflammatory etiology were obtained, and they revealed considerably higher amounts of VEGF-A isoforms compared to specimens with idiopathic etiology.

14

Reciprocal regulation between nitric oxide and vascular endothelial growth factor in angiogenesis

75%

Kimura H., Esumi H.

Acta Biochimica Polonica

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2003

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tom 50

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nr 1

Physiologically, angiogenesis is tightly regulated, or otherwise it leads to pathological processes, such as tumors, inflammatory diseases, gynecological diseases and diabetic retinopathy. The vascular endothelial growth factor (VEGF) is a potent and critical inducer of angiogenesis. The VEGF gene expression is regulated by a variety of stimuli. Hypoxia is one of the most potent inducers of the VEGF expression. The hypoxia inducible factor 1 (HIF-1) plays as a key transcription factor in hypo- xia-mediated VEGF gene upregulation. Nitric oxide (NO) as well as hypoxia is reported to upregulate the VEGF gene by enhancing HIF-1 activity. The Akt/protein kinase B (PKB) pathway may be involved in NO-mediated HIF-1 activation in limited cell lines. There are some reports of negative effects of NO on HIF-1 and VEGF activity. These conflicting data of NO effects may be attributed mainly to the amount of released NO. Indeed, NO can be a positive or negative modulator of the VEGF gene under the same conditions simply by changing its amounts. The VEGF-mediated angiogenesis requires NO production from activated endothelial NO synthase (eNOS). Activation of eNOS by VEGF involves several pathways including Akt/PKB, Ca2+ /calmodulin, and protein kinase C. The NO-mediated VEGF expression can be regulated by HIF-1 and heme oxygenase 1 (HO-1) activity, and the VEGF-mediated NO production by eNOS can be also modulated by HIF-1 and HO-1 activity, depending upon the amount of produced NO. These reciprocal relations between NO and VEGF may contribute to regulated angiogenesis in normal tissues.

15

Effects of protoporphyrins on production of nitric oxide and expression of vascular endothelial growth factor in vascular smooth muscle cells and macrophages

75%

Jozkowicz A., Dulak J.

Acta Biochimica Polonica

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2003

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tom 50

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nr 1

Heme oxygenase-1 (HO-1), an inducible enzyme degrading heme to biliverdin, iron and carbon monoxide, is involved in regulation of inflammation and angiogenesis. Tin protoporphyrin (SnPPIX) and zinc protoporphyrin (ZnPPIX) are commonly used as competitive inhibitors of HO-1. We aimed to compare the effects of SnPPIX and ZnPPIX on the production of vascular endothelial growth factor (VEGF), activity of inducible nitric oxide synthase (iNOS) and cell viability. All experiments were performed on rat vascular smooth muscle cells and murine RAW264.7 macrophages treated with 3-10 ,uM protoporphyrins. Some cells were additionally stimulated with IL-1β or with lipopolysaccharide. After a 24 h incubation period SnPPIX and ZnPPIX significantly reduced the generation of VEGF in vascular smooth muscle cells and RAW264.7, both in resting and stimulated cells. The inhibitory potentials of both protoporphyrins on VEGF synthesis were very similar. In contrast, analysis of iNOS activity revealed that results obtained with different HO-1 inhibitors are discrepant.

16

Carbon monoxide - A new gaseous modulator of gene expression

75%

Dulak J., Jozkowicz A.

Acta Biochimica Polonica

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2003

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tom 50

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nr 1

Carbon monoxide (CO) is an odorless, tasteless and colorless gas which is generated by heme oxygenase enzymes (HOs). HOs degrade heme releasing equimolar amounts of CO, iron and biliverdin, which is subsequently reduced to bilirubin. CO shares many properties with nitric oxide (NO), an established cellular messenger. Both CO and NO are involved in neural transmission and modulation of blood vessel function, including their relaxation and inhibition of platelet aggregation. CO, like NO, binds to heme proteins, although CO binds only ferrous (Fell) heme, whereas NO binds both ferrous and ferric (Felll). CO enhances the activity of guanylate cyclase although it is less potent than NO. In contrast, CO inhibits other heme proteins, such as catalase or cytochrome P450. The effects of CO on gene expression can be thus varied, depending on the cellular microenvironment and the metabolic pathway being influenced. In this review the regulation of gene expression by HO/CO in the cardiovascular system is discussed. Recent data, derived also from our studies, indicate that HO/CO are significant modulators of inflammatory reactions, influencing the underlying processes such as cell proliferation and production of cytokines and growth factors.

17

VEGF, VEGFR-1 and VEGFR-2 immunoreactivity in the porcine arteries of vascular subovarian plexus [VSP] during the estrous cycle

75%

Postek A., Andronowska A., Doboszynska T., Nieweglowski H., Jankowska K.

Folia Histochemica et Cytobiologica

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2006

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tom 44

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nr 1

18

Effect of ischemic preconditioning on pancreatic regeneration and pancreatic expression of vascular endothelial growth factor and platelet-derived growth factor-A in ischemia-reperfusion-induced pancreatitis

75%

Dembinski A., Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Pawlik W. W., Tomaszewska R., Konturek S. J., Konturek P. C.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 1

Ischemic preconditioning has been shown to protect several organs from ischemia/reperfusion-induced injury. In the pancreas, protective effect of ischemic preconditioning has been shown against pancreatitis evoked by ischemia/reperfusion, as well as by caerulein. However, the effect of ischemic preconditioning on the course of acute pancreatic is unclear. The aim of our study was to evaluate the influence of ischemic preconditioning on pancreatic regeneration and pancreatic presence of platelet-derived growth factor-A (PDGF-A) and vascular endothelial growth factor (VEGF) in the course of ischemia/reperfusion-induced pancreatitis. Methods: In male Wistar rats, ischemic preconditioning of the pancreas was performed by short-term clamping of celiac artery (twice for 5 min with 5 min interval). Acute pancreatitis was induced by clamping of inferior splenic artery for 30 min followed by reperfusion. Rats were sacrificed 1, 5, 12 h or 1, 2, 3, 5, 7, 9 and 21 days after the start of reperfusion. Severity of acute pancreatitis and pancreatic regeneration were determined by biochemical and morphological examination, expression of growth factors was determined by immunohistochemical analysis. Results: In ischemia/reperfusion-induced pancreatitis, the pancreatic damage reached the maximal range between the first and second day of reperfusion, and was followed by subsequent pancreatic regeneration. Ischemic preconditioning alone caused mild passing pancreatic damage and an increase in plasma concentration of pro-inflammatory interleukin-1 and anti-inflammatory interleukin-10. Ischemic preconditioning applied before ischemia/reperfusion-induced pancreatitis reduced morphological and biochemical signs of the pancreatitis-evoked pancreatic damage and accelerated pancreatic regeneration. This effect was associated with improvement of pancreatic blood flow. Ischemic preconditioning, ischemia/reperfusion-induced pancreatitis and their combination increased the presence of VEGF in acinar and islet cells, and immunostaining for PDGF-A in blood vessels. This effect was maximally pronounced after combination of ischemic preconditioning plus pancreatitis and occurred earlier than after pancreatitis alone. Conclusions: Ischemic preconditioning reduces pancreatic damage and accelerates pancreatic healing in the course of ischemia/reperfusion-induced pancreatitis. This effect is associated with the increase in plasma concentration of anti-inflammatory interleukin-10, improvement of pancreatic blood flow and alteration of pancreatic immunohistochemical expression of PDGF-A and VEGF.

19

Biological and pro-angiogenic properties of genetically modified human primary myoblasts overexpressing placental growth factor in in vitro and in vivo studies

63%

Zimna A., Wiernicki B., Kolanowski T., Rozwadowska N., Malcher A., Labedz W., Trzeciak T., Chojnacka K., Bednarek-Rajewska K., Majewski P., Kurpisz M.

Archivum Immunologiae et Therapiae Experimentalis

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2018

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tom 66

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nr 2

20

Combined perioperative plasma endoglin and VEGF-A assessment in colorectal cancer patients

63%

Mysliwiec P., Pawlak K., Kuklinski A., Kedra B.

Folia Histochemica et Cytobiologica

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2009

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tom 47

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nr 2

231-236

Ograniczanie wyników

Role of vascular endothelial growth factor in ovarian physiology - an overview

Vascular endothelial growth factor in systemic lupus erythematosus: relationship to disease activity, systemic organ manifestation, and nailfold capillaroscopic abnormalities

Density of intranodal lymphatics and VEGF-C expression in B-cell lymphoma and reactive lymph nodes

Expression of vascular endothelial growth factor [VEGF] and its receptor FLK-1 in non-small cell lung cancer [NSCLC] - a preliminary report

Placental vascular endothelial growth factor expression in pregnancies complicated by type 1 diabetes

Growth factors and their receptors derived from human amniotic cells in vitro

Manipulation of ovarian follicle development by injecting vascular endothelial growth factor (VEGF) gene

Biological properties of human skeletal myoblasts genetically modified to simultaneously overexpress the pro-angiogenic factors vascular endothelial growth factor-A and fibroblast growth factor-4