A biphasic endothelial stress-survival mechanism regulates the cellular response to vascular endothelial growth factor A

Latham, Antony M.; Odell, Adam F.; Mughal, Nadeem A.; Issitt, Theo; Ulyatt, Clare; Walker, John H.; Homer‐Vanniasinkam, Shervanthi; Ponnambalam, Sreenivasan

doi:10.1016/j.yexcr.2012.06.023

Cited by 6 publications

(4 citation statements)

References 66 publications

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“…The mechanism of the added VEGF that can promote HDPCs proliferation and survive cells from HEMA exposure may involve signal transduction through receptor tyrosine kinases, vascular endothelial growth factor receptor 2 (VEGF-R2), and lead to cell proliferation by either activation of the mitogen-activated protein kinases or MAPK cascade via Raf stimulation or PLC (phospholipase C)-γ. Activation of PI3K (phosphatidylinositol 3-kinase) leads to activation of PKB (protein kinase B) and the cell survival process (7,17). VEGF can also survive cells from hypoxic conditions via the PI3K/Akt/FoxO1 pathway (8).…”

Section: Discussionmentioning

confidence: 99%

“…Another interesting property of VEGF is helping cells survive from stress or hazardous conditions. There have been some studies reporting that VEGF played a role in survival of serum-starved endothelial cells (6,7), as well as survival of these cells in hypoxic conditions (8). A previous study has also revealed that VEGF expression was upregulated in mouse odontoblast-like cells (MDPC-23) exposed to 2-hydroxyethyl methacrylate (HEMA) (9).…”

Section: Introductionmentioning

confidence: 99%

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Effect of recombinant vascular endothelial growth factor and translationally controlled tumor protein on 2‑hydroxyethyl methacrylate‑treated pulp cells

2018

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Vascular endothelial growth factor (VEGF)-A is a potential signaling protein that may promote angiogenesis. VEGF also helps cells survive in stressfull or hazardous conditions. The present study aimed to compare the effect of VEGF with translationally controlled tumor protein (TCTP), an anti‑apoptotic protein in human dental pulp cells (HDPCs), following exposure to 2‑hydroxyethyl methacrylate (HEMA), which is a major residual monomer from resin restorative dental materials. Cell viability, alkaline phosphatase (ALP) activity, mineralization and gene expressions for odontogenic and osteogenic differentiation markers of HDPCs were investigated, following exposure to HEMA and in combination with TCTP and VEGF. The results revealed that TCTP at 1 ng/ml and VEGF at 10 ng/ml significantly promoted the proliferation of HDPCs (P<0.05). TCTP (1 ng/ml) and VEGF (10 ng/ml) maintained the cell viability of 4 mM HEMA‑treated cells at the same percentage as the control. However, cells treated with HEMA+TCTP+VEGF had a lower cell viability than the groups treated with HEMA and TCTP or VEGF alone. TCTP and VEGF promoted cell proliferation, ALP activity and mineralization, and upregulated of DSPP, DMP‑1, BMP‑2, and ALP mRNA expression compared with the control. Furthermore, the HEMA+TCTP and HEMA+VEGF groups had significantly higher percentages of calcium deposition than HEMA‑treated cells (P<0.001). HEMA was cytotoxic to HDPCs, reduced ALP activity and caused the significant downregulation of odontogenic and osteogenic gene expressions (P<0.05). It was concluded that VEGF and TCTP promoted pulp cell growth and the survival of HEMA‑treated cells without synergistic effects. TCTP was required in lower concentrations for these effects. VEGF and TCTP enhanced cell differentiation and mineralization.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of recombinant vascular endothelial growth factor and translationally controlled tumor protein on 2‑hydroxyethyl methacrylate‑treated pulp cells

2018

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“…Under serum starvation conditions, normal endothelium first elevates VEGFR2 levels, an event that is followed by its down-regulation 24hrs thereafter 26 . Meanwhile soluble VEGFR1 (sVEGFR1) decreases during the early phase, and then increases to above normal levels after the 24hr period.…”

Section: Refinement Of Canonical Signalingmentioning

confidence: 99%

“…Although full-length VEGFR1 levels are not altered during this time, increased sVEGFR1 sequesters VEGF in the ECM, preventing it from accessing VEGFR2. Accordingly, the serum-starvation response increases responsiveness to VEGF and pro-survival cues at early stages; but at late stages the effect leads to a reduction in VEGF responsiveness and an increase in apoptosis 26 . Although the direct signaling output of VEGFR1 is unclear, it appears to be highly-valued by the endothelium as a tool to control VEGFR2 function.…”

Section: Refinement Of Canonical Signalingmentioning

confidence: 99%

Canonical and Noncanonical Vascular Endothelial Growth Factor Pathways

Domigan

Ziyad

Iruela‐Arispe

2015

ATVB

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The last five years have witnessed a significant expansion in our understanding of VEGF signaling. In particular, the process of canonical activation of VEGFR tyrosine kinases by homodimeric VEGF molecules have now been broadened by the realization that heterodimeric ligands and receptors are also active participants in the signaling process. While heterodimer receptors were described two decades ago, their impact, along with the effect of additional cell surface partners and novel autocrine VEGF signaling pathways, are only now starting to be clarified. Furthermore, ligand-independent signaling (non-canonical) has been identified which occurs through galectin and gremlin binding, and upon rise of intracellular levels of reactive oxygen species. Activation of the VEGF receptors in the absence of ligand holds immediate implications for therapeutic approaches that exclusively target VEGF. The present review provides a concise summary of the recent developments in both canonical and non-canonical VEGF signaling and places these findings in perspective to their potential clinical and biological ramifications.

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In Vitro Co-culture of Fibroblast and Endothelial Cells to Assess Angiogenesis

Odell

Mannion

2022

Methods in Molecular Biology

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A biphasic endothelial stress-survival mechanism regulates the cellular response to vascular endothelial growth factor A

Cited by 6 publications

References 66 publications

Effect of recombinant vascular endothelial growth factor and translationally controlled tumor protein on 2‑hydroxyethyl methacrylate‑treated pulp cells

Effect of recombinant vascular endothelial growth factor and translationally controlled tumor protein on 2‑hydroxyethyl methacrylate‑treated pulp cells

Canonical and Noncanonical Vascular Endothelial Growth Factor Pathways

In Vitro Co-culture of Fibroblast and Endothelial Cells to Assess Angiogenesis

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