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Cytokine VEGF165

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[#91001-2] Cytokine VEGF165


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(1) Transplantation of CREG modified embryonic stem cells improves cardiac function after myocardial infarction in mice.[TOP]

Pubmed ID :29684345
Publication Date : //
Engraftment of embryonic stem cells (ESC) has been proposed as a potential therapeutic approach for post-infarction cardiac dysfunction. However, only mild function improvement has been achieved due to low survival rate and paracrine dysfunction of transplanted stem cells. Cellular repressor of E1A stimulated genes (CREG) has been reported to be a secreted glycoprotein implicated in promoting survival and differentiation of many cell types. Therefore we hypothesized that transplantation of genetically modified ESC with CREG (CREG-ESC) can improve cardiac function after myocardial infarction in mice. A total of 2 × 10 CREG-ESC or EGFP-ESC were engrafted into the border zone in a myocardial infarction model in mice. Cardiac function, infarct size and fibrosis at 4 weeks, survival of transplanted ESC, apoptosis and cytokine level of heart tissue, and teratoma formation were assessed in vivo. Apoptosis of ESC under inflammatory stimuli and cardiac differentiation of ESC were investigated in vitro. After 4 weeks, we found transplantation of CREG-ESC could significantly improve cardiac function, ameliorate cardiac remodeling, and reduce infarct size and fibrosis area. Transplantation of CREG-ESC remarkably increased ESC survival in the border zone and inhibited apoptosis of cardiomyocytes. Furthermore, the decrease of inflammatory factors (IL-1β, IL-6 and TNF-α) and increase of anti-inflammatory factors (TGF-β, bFGF and VEGF165) in the border zone were higher in CREG-ESC transplanted hearts. Safety evaluation showed that all transplantation at 2 × 10 per heart dose produced no teratoma. Surprisingly, the mice with 3.0 × 10 CREG-ESC transplantation was demonstrated teratoma free without cardiac rhythm disturbances in contrast to 100% teratoma formation and rhythm abnormality for the same dose of EGFP-ESC transplantation. In addition, overexpression of CREG inhibits ESC apoptosis and enhanced their differentiation into cardiomyocytes in vitro. Transplantation of CREG-modified ESC exhibits a favorable survival pattern in infarcted hearts, which translates into a substantial preservation of cardiac function after acute myocardial infarction.

Authors : Zhang Jian, Tian Xiaoxiang, Peng Chengfei, Yan Chenghui, Li Yang, Sun Mingyu, Kang Jian, Gao Erhe, Han Yaling,

(2) Intraocular Penetration of a vNAR: In Vivo and In Vitro VEGF Neutralization.[TOP]

Pubmed ID :29614715
Publication Date : //
Variable new antigen receptor domain (vNAR) antibodies are novel, naturally occurring antibodies that can be isolated from naïve, immune or synthetic shark libraries. These molecules are very interesting to the biotechnology and pharmaceutical industries because of their unique characteristics related to size and tissue penetrability. There have been some approved anti-angiogenic therapies for ophthalmic conditions, not related to vNAR. This includes biologics and chimeric proteins that neutralize vascular endothelial growth factor (VEGF), which are injected intravitreal, causing discomfort and increasing the possibility of infection. In this paper, we present a vNAR antibody against human recombinant VEGF (rhVEGF) that was isolated from an immunized shark. A vNAR called V13, neutralizes VEGF cytokine starting at 75 μg/mL in an in vitro assay based on co-culture of normal human dermal fibroblasts (NHDFs) and green fluorescence protein (GFP)-labeled human umbilical vein endothelial cells (HUVECs) cells. In the oxygen-induced retinopathy model in C57BL/6:Hsd mice, we demonstrate an endothelial cell count decrease. Further, we demonstrate the intraocular penetration after topical administration of 0.1 μg/mL of vNAR V13 by its detection in aqueous humor in New Zealand rabbits with healthy eyes after 3 h of application. These findings demonstrate the potential of topical application of vNAR V13 as a possible new drug candidate for vascular eye diseases.

Authors : Camacho-Villegas Tanya A, Mata-González María Teresa, García-Ubbelohd Walter, Núñez-García Linda, Elosua Carolina, Paniagua-Solis Jorge F, Licea-Navarro Alexei F,

(3) A safety and immunogenicity study of immunization with hVEGF/RFASE in cynomolgus monkeys.[TOP]

Pubmed ID :29519591
Publication Date : //
Vascular endothelial growth factor (VEGF) is pivotal in tumor angiogenesis and therapies targeting the VEGF axis are widely used in the clinic for the treatment of cancer. We have developed a therapeutic vaccine targeting human (h)VEGF. hVEGF/RFASE is based on the truncated protein hVEGF as antigen formulated in an oil-in-water emulsion containing the sulpholipopolysaccharide RFASE as adjuvant. Here we describe the toxicity and immunogenicity of this therapeutic vaccine in cynomolgus monkeys.

Authors : Wentink Madelon Q, Verheul Henk M W, Griffioen Arjan W, Schafer Kenneth A, McPherson Susan, Early Richard J, van der Vliet Hans J, de Gruijl Tanja D,

(4) Experimental variation of the level and the ratio of angiogenic and osteogenic signaling affects the spatiotemporal expression of bone-specific markers and organization of bone formation in ectopic sites.[TOP]

Pubmed ID :28936783
Publication Date : //
The aim of the present study was to test the hypothesis that the ratio of angiogenic and osteogenic signaling affects ectopic bone formation when delivered in different amounts.

Authors : Moser Norman, Goldstein Jan, Kauffmann Phillip, Epple Matthias, Schliephake Henning,

(5) Inhibiting Vascular Endothelial Growth Factor in Injured Intervertebral Discs Attenuates Pain-Related Neuropeptide Expression in Dorsal Root Ganglia in Rats.[TOP]

Pubmed ID :28874973
Publication Date : //
An experimental animal study.

Authors : Sato Jun, Inage Kazuhide, Miyagi Masayuki, Sakuma Yoshihiro, Yamauchi Kazuyo, Koda Masao, Furuya Takeo, Nakamura Junichi, Suzuki Miyako, Kubota Go, Oikawa Yasuhiro, Sainoh Takeshi, Fujimoto Kazuki, Shiga Yasuhiro, Abe Koki, Kanamoto Hirohito, Inoue Masahiro, Kinoshita Hideyuki, Norimoto Masaki, Umimura Tomotaka, Takahashi Kazuhisa, Ohtori Seiji, Orita Sumihisa,

(6) VEGF synthesis is induced by prostacyclin and TGF-β in distal lung fibroblasts from COPD patients and control subjects: Implications for pulmonary vascular remodelling.[TOP]

Pubmed ID :28834088
Publication Date : //
Involvement of pulmonary vascular remodelling is a characteristic sign in COPD. Vascular mediators such as vascular endothelial growth factor (VEGF) and prostacyclin may regulate fibroblast activity. The objective was to study the synthesis of VEGF and interactions with prostacyclin and transforming growth factor (TGF)-β in lung fibroblasts from patients with COPD and healthy control subjects. To further explore the autocrine role of synthesized VEGF on fibroblast activity, studies were performed in human lung fibroblasts (HFL-1).

Authors : Westergren-Thorsson Gunilla, Bagher Mariam, Andersson-Sjöland Annika, Thiman Lena, Löfdahl Claes-Göran, Hallgren Oskar, Bjermer Leif, Larsson-Callerfelt Anna-Karin,

(7) MicroRNA-143 and -145 modulate the phenotype of synovial fibroblasts in rheumatoid arthritis.[TOP]

Pubmed ID :28775366
Publication Date : //
Fibroblast-like synoviocytes (FLSs) constitute a major cell subset of rheumatoid arthritis (RA) synovia. Dysregulation of microRNAs (miRNAs) has been implicated in activation and proliferation of RA-FLSs. However, the functional association of various miRNAs with their targets that are characteristic of the RA-FLS phenotype has not been globally elucidated. In this study, we performed microarray analyses of miRNAs and mRNAs in RA-FLSs and osteoarthritis FLSs (OA-FLSs), simultaneously, to validate how dysregulated miRNAs may be associated with the RA-FLS phenotype. Global miRNA profiling revealed that miR-143 and miR-145 were differentially upregulated in RA-FLSs compared to OA-FLSs. miR-143 and miR-145 were highly expressed in independent RA-FLSs. The miRNA-target prediction and network model of the predicted targets identified insulin-like growth factor binding protein 5 (IGFBP5) and semaphorin 3A (SEMA3A) as potential target genes downregulated by miR-143 and miR-145, respectively. IGFBP5 level was inversely correlated with miR-143 expression, and its deficiency rendered RA-FLSs more sensitive to TNFα stimulation, promoting IL-6 production and NF-κB activity. Moreover, SEMA3A was a direct target of miR-145, as determined by a luciferase reporter assay, antagonizing VEGF-induced increases in the survival, migration and invasion of RA-FLSs. Taken together, our data suggest that enhanced expression of miR-143 and miR-145 renders RA-FLSs susceptible to TNFα and VEGF stimuli by downregulating IGFBP5 and SEMA3A, respectively, and that these miRNAs could be therapeutic targets.

Authors : Hong Bong-Ki, You Sungyong, Yoo Seung-Ah, Park Dohyun, Hwang Daehee, Cho Chul-Soo, Kim Wan-Uk,

(8) Endocultivation of Scaffolds with Recombinant Human Bone Morphogenetic Protein-2 and VEGF in the Omentum Majus in a Rabbit Model.[TOP]

Pubmed ID :28762869
Publication Date : //
The reconstruction of defects in the mandible are still challenging. Despite several adequate microvascular bone reconstruction techniques, there is a need for ectopic bone endocultivation without drawbacks by donor-site morbidity. The omentum majus is described as a good vascularized fleece with undifferentiated cells with potential for bone culturing. In the omentum majus of six rabbits, two hydroxyapatite blocks were incorporated for 12 weeks each. The blocks were prepared with recombinant human bone morphogenetic protein-2 (rhBMP-2) or VEGF + rhBMP-2 and wrapped into the omentum. For ectopic bone endocultivation observation computed tomography (CT) scans were performed, and fluorescence markers were applied. After harvesting the block, histological sections were performed with hematoxylin and eosin and toluidine blue staining. In the CT scans, the Hounsfield units of the blocks increased within the trail. In some sections, new bone formation was observed within the hydroxyapatite blocks, however, the histological staining showed soft-tissue invasion only, no gross bone formation was observed. The ectopic bone endocultivation in the omentum majus is technically a good approach. An adequate mixture of osteoinductive proteins is still missing.

Authors : Birkenfeld Falk, Sengebusch Andre, Völschow Chiara, Naujokat Hendrik, Möller Björn, Wieker Henning, Wiltfang Jörg,

(9) Physicochemical regulation of TGF and VEGF delivery from mesoporous calcium phosphate bone substitutes.[TOP]

Pubmed ID :28703639
Publication Date : //
Determination of the physicochemical parameters governing growth factors (GFs) adsorption and release from mesoporous calcium phosphate ceramics.

Authors : Möller-Siegert Janina, Parmentier Julien, Laquerrière Patrice, Ouadi Ali, Raisslé Olivier, Jallot Edouard, Nedelec Jean-Marie, Vix-Guterl Cathie, Anselme Karine,

(10) Vascular endothelial growth factor is neuroprotective against ischemic brain injury by inhibiting scavenger receptor A expression on microglia.[TOP]

Pubmed ID :28632969
Publication Date : //
Vascular endothelial growth factor (VEGF) is a secreted mitogen associated with angiogenesis. VEGF has long been thought to be a potent neurotrophic factor for the survival of spinal cord neurons. However, the role of VEGF in the regulation of ischemic brain injury remains unclear. In this study, rats were subjected to MCAO (middle cerebral artery occlusion) followed by intraperitoneal injection of VEGF165 (10 mg/kg) immediately after surgery and once daily until the day 10. The expression of target genes was assayed using qPCR, western blot and immunofluorescence to investigate the role of VEGF165 in regulating ischemic brain injury. We found that VEGF165 significantly inhibited MCAO-induced up-regulation of Scavenger receptor class A (SR-A) on microglia in a VEGFR1-dependent manner. VEGF165 inhibited lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines IL-1β, tumor necrosis factor alpha (TNF-α) and iNOS in microglia. More importantly, the role of VEGF165 in inhibiting neuroinflammation is partially abolished by SR-A over-expression. SR-A further reduced the protective effect of VEGF165 in ischemic brain injury. These data suggest that VEGF165 suppresses neuroinflammation and ischemic brain injury by inhibiting SR-A expression, thus offering a new target for prevention of ischemic brain injury.

Authors : Xu Zheng, Han Kaiwei, Chen Jigang, Wang Chunhui, Dong Yan, Yu Mingkun, Bai Rulin, Huang Chenguang, Hou Lijun,