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Cytokine VEGF165

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[#91001-3] 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) 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,



(4) 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,



(5) [Comparison of differentiated endothelial cells from the embryonic stem cells with human umbilical vein endothelial cells].[TOP]

Pubmed ID :28490693
Publication Date : //
To compare the differentiated endothelial cells from the embryonic stem cells in vitro with human umbilical vein endothelial cells (HUVECs).
 Methods: Induction of the stem cells HUES9 to endothelial cells follows 2 steps. Stem cells were treated with CHIR99021 (10 µmol/L) and bone morphogenetic protein 4 (25 ng/mL) for 3 days to keep mesoderm state, then subsequent exposure them to VEGF165 (200 ng/mL) and Forskolin (2 µmol/L) to differentiate into endothelial cells. The morphology of differentiated endothelial cells were compared with HUVECs. The surface marker CD144 on differentiated cells and HUVECs were detected. The capabilities of two types of endothelial cells in migration and angiogenesis were examined.
 Results: The differentiated endothelial cells show the same morphology with HUVECs. After 6 days of differentiation, the efficiency reached 73.4%. The positive percentage of CD144 for the differentiated endothelial cells and HUVECs was 86.6% and 94.4%, respectively. Both of them show capabilities of migration and angiogenesis, especially when they were treated with SB431542 to inhibit TGF-β signal pathway.
 Conclusion: The method for induction of stem cells to endothelial cells is productivity and it can be used for further study.

Authors : Wang Yangui, Mao Xiaoxiao, Yang Tianlun,



(6) Novel pegylated interferon-β as strong suppressor of the malignant ascites in a peritoneal metastasis model of human cancer.[TOP]

Pubmed ID :28129467
Publication Date : //
Malignant ascites manifests as an end-stage event during the progression of a number of cancers and lacks a generally accepted standard therapy. Interferon-β (IFN-β) has been used to treat several cancer indications; however, little is known about the efficacy of IFN-β on malignant ascites. In the present study, we report on the development of a novel, engineered form of human and murine IFN-β, each conjugated with a polyethylene glycol molecule (PEG-hIFN-β and PEG-mIFN-β, respectively). We provide evidence that these IFN-β molecules retain anti-viral potency comparable to unmodified IFN-β in vitro and manifested improved pharmacokinetics in vivo. Interestingly, PEG-mIFN-β significantly inhibited the accumulation of ascites fluid and vascular permeability of the peritoneal membrane in models of ovarian cancer and gastric cancer cell xenograft mice. We further show that PEG-hIFN-β directly suppresses VEGF -induced hyperpermeability in a monolayer of human vascular endothelial cells and that PEG-mIFN-β enhanced gene expression for a number of cell adhesion related molecules in mouse vascular endothelial cells. Taken together, these findings unveil a hitherto unrecognized potential of IFN-β in maintaining vascular integrity, and provide proof-of-mechanism for a novel and long-acting pegylated hIFN-β for the therapeutic treatment of malignant ascites.

Authors : Iwamura Tomokatsu, Narumi Hideki, Suzuki Tomohiko, Yanai Hideyuki, Mori Katsuyuki, Yamashita Koji, Tsushima Yoshiaki, Asano Tomomi, Izawa Akiko, Momen Shinobu, Nishimura Kazumi, Tsuchiyama Hiromi, Uchida Masashi, Yamashita Yuji, Okano Kiyoshi, Taniguchi Tadatsugu,



(7) Inhibition of VEGF165/VEGFR2-dependent signaling by LECT2 suppresses hepatocellular carcinoma angiogenesis.[TOP]

Pubmed ID :27507763
Publication Date : //
Hepatocellular carcinoma (HCC) relies on angiogenesis for growth and metastasis. Leukocyte cell-derived chemotaxin 2 (LECT2) is a cytokine and preferentially expressed in the liver. Previous studies have found that LECT2 targets to both immune and tumor cells to suppress HCC development and vascular invasion. Although LECT2 did not affect HCC cells growth in vitro, it still suppressed HCC xenografts growth in immune-deficient mice, suggesting other cells such as stroma cells may also be targeted by LECT2. Here, we sought to determine the role of LECT2 in tumor angiogenesis in HCC patients. We found that LECT2 expression inhibited tumor growth via angiogenesis in the HCC xenograft model. Specifically, we demonstrated that recombinant human LECT2 protein selectively suppressed vascular endothelial growth factor (VEGF)165-induced endothelial cell proliferation, migration, and tube formation in vitro and in vivo. Mechanistically, LECT2 reduced VEGF receptor 2 tyrosine phosphorylation and its downstream extracellular signal-regulated kinase and AKT phosphorylation. Furthermore, LECT2 gene expression correlated negatively with angiogenesis in HCC patients. Taken together, our findings demonstrate that LECT2 inhibits VEGF165-induced HCC angiogenesis through directly binding to VEGFR2 and has broad applications in treating VEGF-mediated solid tumors.

Authors : Chen Chi-Kuan, Yu Wen-Hsuan, Cheng Tsu-Yao, Chen Min-Wei, Su Chia-Yi, Yang Yi-Chieh, Kuo Tsang-Chih, Lin Ming-Tsan, Huang Ya-Chi, Hsiao Michael, Hua Kuo-Tai, Hung Mien-Chie, Kuo Min-Liang,



(8) Elevated expression levels of serum insulin-like growth factor-1, tumor necrosis factor-α and vascular endothelial growth factor 165 might exacerbate type 2 diabetic nephropathy.[TOP]

Pubmed ID :27218216
Publication Date : //
The present study aimed to determine the associations between expressions of insulin-like growth factor-1 (IGF-1), tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor 165 (VEGF ) in serum, and occurrence and development of type 2 diabetic nephropathy (DN).

Authors : Li Xiang, Wu Ting-Ting, Chen Juan, Qiu Wen,



(9) Angiogenesis related genes NOS3, CD14, MMP3 and IL4R are associated to VEGF gene expression and circulating levels in healthy adults.[TOP]

Pubmed ID :26437765
Publication Date : //
Vascular endothelial growth factor (VEGF) plays a key role in angiogenesis. The aim was to assess the genetic connections between the angiogenesis-related NOS3, CD14, MMP3, IL4R, IL4 genes and VEGF expression and plasma levels.

Authors : Saleh Abdelsalam, Stathopoulou Maria G, Dadé Sébastien, Ndiaye Ndeye Coumba, Azimi-Nezhad Mohsen, Murray Helena, Masson Christine, Lamont John, Fitzgerald Peter, Visvikis-Siest Sophie,



(10) Proinflammatory Cytokines Increase Vascular Endothelial Growth Factor Expression in Alveolar Epithelial Cells.[TOP]

Pubmed ID :26424968
Publication Date : //
Vascular endothelial growth factor (VEGF) is an endothelial permeability mediator that is highly expressed in lung epithelium. In nonlung cells proinflammatory cytokines have been shown to increase VEGF expression, but their effects on lung epithelium remain unclear. We hypothesized that increases in alveolar epithelial cell VEGF RNA and protein expression occur after exposure to proinflammatory cytokines. We tested this using human alveolar epithelial cells (A549) stimulated with 5 proinflammatory cytokines. VEGF RNA expression was increased 1.4-2.7-fold in response to IL-1, IL-6, IL-8, TNF-α, or TGF-β over 6 hours, with TGF-β having the largest response. TNF-α increased VEGF RNA as early as 1 hour. A mix of IL-1, IL-6, and IL-8 had effects similar to IL-1. TNF-α increased protein expression as early as 4 hours and had a sustained effect at 16 hours, whereas IL-1 did not increase protein expression. Only VEGF165 was present in cultured A549 cells, yet other isoforms were seen in human lung tissue. Increased expression of VEGF in alveolar epithelial cells occurs in response to proinflammatory cytokines. Increased VEGF expression likely contributes to the pathogenesis of inflammatory lung diseases and to the angiogenic phenotype of lung cancer, a disease typically preceded by chronic inflammation.

Authors : Maloney James P, Gao Li,