Vascular endothelial growth factors: A comparison between invertebrates and vertebrates

Kipryushina, Yulia O.; Yakovlev, Konstantin V.; Odintsova, N. A.

doi:10.1016/j.cytogfr.2015.04.001

Cited by 20 publications

(14 citation statements)

References 98 publications

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“…In fact, it is a single factor now referred to as VEGF (or VEGF-A), encoded by the VEGFA gene [65] . In humans, 5 homolog genes ( VEGFA, VEGFB, VEGFV, VEGFD , and PGF ) constitute the VEGF family, which belongs to the VEGF/PDGF superfamily [66] that appeared early in the evolution in the common ancestor of Eumetazoan [67] . VEGF-A is an endothelial specific growth factor, with a signal peptide for secretion, a heparin-binding site and a highly conserved cystine-knot domain involved in the binding of VEGF to their receptors [68] .…”

Section: Mechanisms Of Plaque Neovascularizationmentioning

confidence: 99%

Angiogenesis in the atherosclerotic plaque

et al. 2017

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Atherosclerosis is a multifocal alteration of the vascular wall of medium and large arteries characterized by a local accumulation of cholesterol and non-resolving inflammation. Atherothrombotic complications are the leading cause of disability and mortality in western countries. Neovascularization in atherosclerotic lesions plays a major role in plaque growth and instability. The angiogenic process is mediated by classical angiogenic factors and by additional factors specific to atherosclerotic angiogenesis. In addition to its role in plaque progression, neovascularization may take part in plaque destabilization and thromboembolic events. Anti-angiogenic agents are effective to reduce atherosclerosis progression in various animal models. However, clinical trials with anti-angiogenic drugs, mainly anti-VEGF/VEGFR, used in anti-cancer therapy show cardiovascular adverse effects, and require additional investigations.

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Section: Mechanisms Of Plaque Neovascularizationmentioning

confidence: 99%

Angiogenesis in the atherosclerotic plaque

et al. 2017

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“…After decapitation, the ectoderm and endoderm stretch over the open wound and form the round shaped apical cap. Tentacle buds appear in the tentacle zone within [30][31][32][33][34][35][36] hpd. Further, the apical cap forms a dome shaped structure from which arises the hypostome [8].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, VEGF signaling also regulates cell proliferation and migration, vascular permeability, regeneration, tumour progression, etc. [33]. Homologs of VEGF and VEGFR are present in the jelly fish Podocoryne carnea and role of VEGF signaling in tube formation has been proposed [29].…”

Section: Discussionmentioning

confidence: 99%

VEGF and FGF signaling during head regeneration in hydra

Turwankar

Ghaskadbi

2019

Preprint

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Background: Vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) signaling pathways play important roles in the formation of the blood vascular system and nervous system across animal phyla. We have earlier reported VEGF and FGF from Hydra vulgaris Ind-Pune, a cnidarian with a defined body axis, an organized nervous system and a remarkable ability of regeneration. We have now identified three more components of VEGF and FGF signaling pathways from hydra. These include FGF-1, FGF receptor 1 (FGFR-1) and VEGF receptor 2 (VEGFR-2) with a view to deciphering their possible roles in regeneration. Methods:In silico analysis of proteins was performed using Clustal omega, Swiss model, MEGA 7.0, etc. Gene expression was studied by whole mount in situ hybridization. VEGF and FGF signaling was inhibited using specific pharmacological inhibitors and their effects on head regeneration were studied. Results: Expression patterns of the genes indicate a possible interaction between FGF-1 andFGFR-1 and also VEGF and VEGFR-2. Upon treatment of decapitated hydra with pharmacological inhibitor of FGFR-1 or VEGFR-2 for 48 hours, head regeneration was delayed in treated as compared to untreated, control regenerates. When we studied the expression of head specific genes HyBra1 and HyKs1 and tentacle specific gene HyAlx in control and treated regenerates using whole mount in situ hybridization, expression of all the three genes was found to be adversely affected in treated regenerates. Conclusions:The results suggest that VEGF and FGF signaling play important roles in regeneration of hypostome and tentacles in hydra.

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“…The functions of VEGFs in wound repair has been extensively studied including angiogenesis, wound closure, epidermal repair, and granulation tissue formation [ 17 ]. These effects are mediated by binding to tyrosine kinase receptors (i.e., the VEGFRs) located on endothelial cells, involving the stimulation of cell proliferation, migration, survival, tube formation and regulation of vascular permeability [ 17 , 23 ]. Despite the absence of blood vessels or blood cells, VEGF/VEGFR signaling has also been found in invertebrates.…”

Section: Discussionmentioning

confidence: 99%

Tentacle extract from the jellyfish Cyanea capillata increases proliferation and migration of human umbilical vein endothelial cells through the ERK1/2 signaling pathway

et al. 2017

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Wound healing is a complex biological process, and current research finds that jellyfish have a great capacity for promoting growth and healing. However, the underlying mechanisms remain unclear. Thus, this study was conducted to investigate the molecular mechanisms and effects of a tentacle extract (TE) from the jellyfish Cyanea capillata (C. capillata) on cell proliferation and migration in human umbilical vein endothelial cells (HUVECs). First, our results showed that TE at the concentration of 1 μg/ml could promote cell proliferation over various durations, induce a transition of the cells from the G1-phase to the S/G2-phase of the cell cycle, and increase the expression of cell cycle proteins (CyclinB1 and CyclinD1). Second, we found that TE could activate the PI3K/Akt, ERK1/2 and JNK MAPK signaling pathways but not the NF-κB signaling pathway or the apoptosis signaling cascade. Finally, we demonstrated that the TE-induced expression of cell cycle proteins was decreased by ERK1/2 inhibitor PD98059 but not by PI3K inhibitor LY294002 or JNK inhibitor SP600125. Similarly, the TE-enhanced migration ability of HUVECs was also markedly attenuated by PD98059. Taken together, our findings indicate that TE-induced proliferation and migration in HUVECs mainly occurred through the ERK1/2 MAPK signaling pathway. These results are instructively important for further research on the isolation and purification of growth-promoting factors from C. capillata and are hopeful as a means to improve human wound repair in unfavorable conditions.

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Vascular endothelial growth factors: A comparison between invertebrates and vertebrates

Cited by 20 publications

References 98 publications

Angiogenesis in the atherosclerotic plaque

Angiogenesis in the atherosclerotic plaque

VEGF and FGF signaling during head regeneration in hydra

Tentacle extract from the jellyfish Cyanea capillata increases proliferation and migration of human umbilical vein endothelial cells through the ERK1/2 signaling pathway

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