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Codelivery in Nanoparticle-based siRNA for Cancer Therapy
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
Another strategy to reduce cytotoxicity of high molecular weight PEI is by grafting stearic acid (SA) to PEI through carbodiimide conjugation using 1-ethyl-3-(3-dimethylamino-propyl) carbodiimide (EDC) reaction [132]. PEI-SA micelles were formed using the oil in water (o/w) solvent evaporation method, obtaining small (≈51 nm) and cationic (≈64 mV) micelles. These micelles contain both a hydrophobic core that can encapsulate a hydrophobic drug and a hydrophilic cationic shell capable of complexing siRNA. DOX was encapsulated into the micelles by mild agitation. siRNA against the vascular endothelial growth factor (VEGF) was complexed onto the nanoparticle surface. VEGF is a growth factor over secreted by tumors to force the formation of new blood vessels by stimulating the growth and division of endothelial cells to provide oxygen-rich blood to tumor cells. This process is known as angiogenesis, and it has been proven to be necessary for the tumor to survive. By blocking the formation of new blood vessels irrigating the tumor with oxygen, tumor growth can be stopped. PEI-SA/DOX reduced the volume of the tumor down to 13% relative to the control. When using PEI-SA/DOX/viVEGF, the tumor was reduced down to 56.7%.
Controlled Delivery of Angiogenic Proteins
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
Binita Shrestha, Jacob Brown, Eric M. Brey
Vascular Endothelial Growth Factors (VEGFs) are a family of factors that are required for angiogenesis and/or lymphangiogenesis (formation of lymphatic vessels). The VEGF family consists of a number of members, including VEGF-A (which has many isoforms), VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PIGF) [20]. Each of these members play important, but often different, roles in biological processes. For example, VEGF-A binds with VEGFR-1 to regulate normal and pathological angiogenesis. VEGF-A also binds with VEGFR-2 to modulate growth, migration, survival, and permeability of ECs [21] and stimulates ECs to release other growth factors essential to activate surrounding cells [22]. VEGF-C and VEGF-D and their receptor VEGFR-3 have been reported to regulate lymphangiogenesis. There is also a subgroup of VEGF isolated from snake venom, VEGF-F. VEGF-F regulates vascular permeability, angiogenesis, and blood pressure [23]. PIGF binds specifically to VEGFR-1 and regulates vascular events in both angiogenesis and vasculogenesis [24].
Principles and Biological Pathways to Tissue Regeneration: The Tissue Regenerative Niche
Published in Claudio Migliaresi, Antonella Motta, Scaffolds for Tissue Engineering, 2014
Ranieri Cancedda, Claudia Lo Sicco
[Ferrara et al., 2003]. The HIF-1 transcription complex can induce a 30-fold increase of VEGF expression. Different members of the VEGF family and different spliced form of the same VEGF protein have been identified (VEGF-A, VEGF-B, VEGF-C, placenta-derived growth factor). These variants interact at variable efficiency with the endothelial tyrosine kinase VEGF receptors (VEGFR-1, VEGFR-2, VEGFR-3) resulting in different final biological effects. VEGF family members promote angiogenesis by activating both cell protein kinases and the endothelial nitric oxide synthase [Silvestre et al., 2003]. Other angiogenic factors include angiopoietin-2/ angiopoietin-1 [Phelan et al., 1998; Kietzmann et al., 1999], Tie2 [Kuwabara et al., 1995], PDGF [Negus et al., 1998; Wykoff et al., 2000], basic fibroblast growth factor (bFGF) [Sakuda et al., 1992], and MCP-1 [Fuentes et al., 1995]. These factors not only increase vascular permeability and endothelial sprouting, but also promote endothelial cell recruitment, proliferation, and migration as well as the enhancement of endothelial lumen assembly. Factors that promote endothelial cell recruitment, proliferation, migration are named direct angiogenic factors. Differently, indirect angiogenic factors function upstream the direct angiogenic factors, promoting their secretion by cells recruited into the wound site.
Diabetic retinopathy progression associated with haplotypes of two VEGFA SNPs rs2010963 and rs699947
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Haider Ali Alnaji, Rabab Omran, Aizhar H. Hasan, Mohammed Qasim Al Nuwaini
as rs2010963 have been strongly linked with Recent meta-analysis findings indicated that rs2010963 was associated with PDR in the overall population VEGF protein in the blood [25]. The VEGF protein is a potent angiogenic agent in various diseases. It has been established that elevated serum and vitreous levels of VEGF in the presence of retinopathy are closely associated with proliferative diabetic retinopathy [26]. A study from Egypt explored the association between rs699947 SNP and the susceptibility of DR, and it found no significant association between them. This result is consistent with our findings [27]. Different studies also revealed no association between the presence of rs699947 SNP and the risk of DR [28]. In a previous meta-analysis, the rs699947 in Asian individuals with type 2 diabetes are more likely to be associated with DR but not in white people [29]. While a meta-analysis from China recognizes the reverse association that rs699947 polymorphism is strongly connected with DR after adjusting for outliers, rs2010963 polymorphism may not be linked to DR [30]. Different meta-analyses on rs2010963; one revealed an association while the other did not [31,32].
Gene variants previously associated with reduced soft tissue injury risk: Part 1 – independent associations with elite status in rugby
Published in European Journal of Sport Science, 2023
Jon Brazier, Mark R. Antrobus, Adam J. Herbert, Peter C. Callus, Georgina K. Stebbings, Stephen H. Day, Shane M. Heffernan, Liam P. Kilduff, Mark A. Bennett, Robert M. Erskine, Stuart. M. Raleigh, Malcolm Collins, Yannis. P. Pitsiladis, Alun G. Williams
Other genes and pathways have been associated with increased risk of soft tissue injury. One being angiogenesis which is essential during the repair and remodelling of injured tendons and has been implicated in matrix remodelling following mechanical loading Petersen et al. (2004). Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen that stimulates angiogenesis with the A isoform, coded by VEGFA, thought to be the most potent. Petersen et al. (2004) The majority of the biological effects of VEGFA are facilitated via its receptor: Kinase insert-domain receptor (KDR). Genes that encode for both of these proteins (VEGFA and KDR) have previously been investigated for their associations with ACL rupture and Achilles tendinopathy, with a VEFGA gene polymorphism (rs699947) associated with both forms of injury Rahim et al. (2014), Rahim et al. (2016) Additionally, several genetic variants recently identifed in a genome-wide assocation study (GWAS) for Achilles tendon and ACL tears and tendinopathy, Kim et al. (2017) are worthy of future study: COLGALT1 rs8090 is potentially important in the aetiology of connective tissue disorders due to post-translational modifications possibly disrupting collagen modifying enzymes; Schegg, Hülsmeier, Rutschmann, Maag, and Hennet (2009) NID1 rs4660148 encodes a member of the nidogen family thought to play a role in the development of the ECM; Ho, Böse, Mokkapati, Nischt, and Smyth (2008) MIR608 rs4919510 encodes a small non-coding RNA involved in gene silencing and translational repressions Matzke and Birchler (2005).
VEGF loaded porcine decellularized adipose tissue derived hydrogel could enhance angiogenesis in vitro and in vivo
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Kaituo Liu, Ming Zhao, Yan Li, Liang Luo, Dahai Hu
Several growth factors are played vital roles in wound healing process like VEGF, bFGF [1]. Numerous proangiogenic factors have been identified in which VEGF is a key mediator that promotes angiogenesis. VEGF-A is the most effective factor to induce angiogenesis among the VEGF family. VEGF could interact with VEGFR-1 and VEGFR-2, which VEGFR-2 is mainly expressed on vascular endothelial cells and VEGFR-1 is expressed in several cells like macrophages, fibroblasts [16]. Several researches showed that VEGF could modulate inflammation reactions through modulating polarization of macrophages [17,18]. Based on these reasons, VEGF could be one of the most promising growth factors facilitated in wound healing. However, VEGF associated therapies were not applied in wound related clinical trials for the reason that VEGF could lose bioactivity soon without long-lasting effect. Otherwise, VEGF has the heparin binding domain which could interact with heparin and heparin could be covalently-linked to collagens through EDC/NHS reaction [19,20]. Through this modification of materials, we can reach this goal to restore VEGF and release VEGF slowly.