Vascular endothelial growth factor receptor-1 (VEGFR-1) signaling enhances angiogenesis in a surgical sponge model.

Park, Keiichi; Aoki, Hideki; Yoshiya, Ikuto; Kashiwagi, Seizaburo; Yamazaki, Yasuharu; Shibuya, Masabumi; Kitasato, Hidero; Murakami, Masataka

doi:10.1016/j.biopha.2016.01.005

Cited by 17 publications

(21 citation statements)

References 38 publications

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“…35,36 Via binding to VEGFR-1/ 2, VEGF significantly increases the number of CD31 + vessels in an in vivo angiogenesis model. 37 Similarly, after the vessel rupture-caused stroke, the findings in this study that both the HIF-1α and VEGFA mRNA levels increased and are positively associated with CD31 mRNA levels suggest that hypoxia leads to HIF-1a, VEGFA expression and consequently angiogenesis initiation. The transplantation of VEGF-over-expressing neural stem cells leads to angiogenesis and functional recovery in mouse stroke model.…”

Section: A B Csupporting

confidence: 55%

<p>Effect of the Recombinant Adenovirus-Mediated HIF-1 Alpha on the Expression of VEGF in the Hypoxic Brain Microvascular Endothelial Cells of Rats</p>

Jin¹,

Zou²,

Tao³

et al. 2020

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To investigate the effect of recombinant adenovirus-mediated HIF-1 alpha (HIF-1α) on the expression of vascular endothelial growth factor (VEGFA) and HIF-1α in hypoxic brain microvascular endothelial cells (BMEC) in rats. Methods: Primary cultured rat BMEC in vitro were treated without or with either recombinant adenovirus-mediated hypoxia-inducible factor-1 alpha (AdHIF-1α) or recombinant adenovirus empty vector (Ad) in the presence of CoCl 2 (simulating hypoxia conditions), or were grown under normoxia conditions. The expression of VEGFA and HIF-1α was analyzed at 12h, 24h, 48h and 72h incubation time, respectively. We also accessed a GEO dataset of stroke to analyze in vivo the alteration of HIF-1α and VEGFA expression, and the correlations between HIF-1α, VEGFA and CD31 mRNA levels in vascular vessels after stroke. Results: VEGFA and HIF-1α expression were significantly higher in at each time point in the AdHIF-1α than other groups (p<0.05), whereas the Ad group and hypoxia group, showed no statistically significant difference (p>0.05). Moreover, VEGFA and HIF-1α levels were significantly higher in BMEC under hypoxia conditions than normoxia conditions (p <0.05). Both HIF-1α and VEGFA expression significantly increased after stroke in vivo with 1.30 and 1.57 fold-change in log2, respectively. There were significantly positive associations between HIF-1α, VEGFA and CD31 mRNA levels in vivo after stroke. Conclusion: Hypoxia-induced HIF-1α and VEGFA expression in vascular vessels, and recombinant AdHIF-1α could up-regulate VEGFA, and enhance HIF-1ααlevels in BMEC in vitro, which may play an important role in the recovery of stroke.

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Section: A B Csupporting

confidence: 55%

<p>Effect of the Recombinant Adenovirus-Mediated HIF-1 Alpha on the Expression of VEGF in the Hypoxic Brain Microvascular Endothelial Cells of Rats</p>

Jin¹,

Zou²,

Tao³

et al. 2020

NDT

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show abstract

“…Although these receptors are highly similar in amino acid sequence, different VEGFRs have disparate functions and play key role in different pathological processes and signal transductions [40]. Previous studies indicated that VEGFR-1 was mainly involved in angiogenesis [41] and VEGFR-3 was involved in migration and invasion in cancer cells [42], while VEGFR-2 was closely involved with inflammation response [43]. It has been reported that VEGF activated VEGFR-2 to promote its auto-phosphorylation to generate p-VEGFR-2 [44], which exerted specific effects on intercellular permeability [45].…”

Section: Discussionmentioning

confidence: 99%

Propofol attenuated TNF-α-modulated occludin expression by inhibiting Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway in hCMEC/D3 cells

et al. 2019

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Background: The levels of tight junction proteins (TJs), especially occludin, correlate with blood-brain barrier (BBB) disruption caused by inflammation in central nervous system (CNS). It has been reported that propofol, the most commonly used anesthetic, could inhibit inflammation response in CNS. In this study, we investigated the effects of tumor necrosis factor-α (TNF-α) and propofol on occludin expression in human cerebral microvascular endothelial cell line, D3 clone (hCMEC/D3 cells), and explored the underlying mechanisms. Methods: The hCMEC/D3 cells were treated with propofol, followed by TNF-α. The expression and phosphorylation of Hif-1α, VEGF, VEGFR-2, ERK, p38MAPK and occludin were measured by Western blot analysis. The cell viability of hCMEC/D3 cells was measured by cell counting kit-8. Results: TNF-α (10 ng/ml, 4 h) significantly decreased the expression of occludin, which was attenuated by propofol (25 μM). TNF-α induced Hif-1α/VEGF/VEGFR-2/ERK signaling pathway, while propofol could inhibit it. TNF-α induced the phosphorylation of p38MAPK, while propofol had no effect on it. In addition, the inhibitors of Hif-1α, VEGFR-2, and ERK could reduce the effect of TNF-α on occludin expression. Conclusion: TNF-α could decrease the expression of occludin via activating Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway, which was attenuated by propofol.

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“…9 VEGF binds to and activates two tyrosine kinase receptors-VEGF receptor-1 (VEGFR-1) and VEGFR-2, although VEGFR-1 has a ten-fold higher affinity to VEGF. 10 On the other hand, VEGFR-1 is known to be a negative regulator of angiogenesis, while elevated levels of VEGFR-1 result in pathological angiogenesis. 11,12 The authors consider that impairment in the regulation of angiogenesis may actually be a cause of the impairment demonstrated in microvascular circulation.…”

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confidence: 99%

Serum Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor-1 Levels in Patients With Fibromyalgia Syndrome

et al. 2019

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Objectives: This study aims to compare the serum vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor-1 (VEGFR-1) levels between patients with fibromyalgia syndrome (FMS) and healthy controls. Patients and methods: The study included 40 female patients (mean age 39.9±10.2 years; range, 22 to 52 years) diagnosed with primary FMS according to the American College of Rheumatology criteria (1990) and 40 healthy female volunteers (mean age 40.9±8.3 years; range, 25 to 53 years). The sociodemographic data of both groups were recorded. The disease duration and the number of tender points were recorded for patients with FMS, and venous blood samples were collected from the two groups for the measurement of serum VEGF and VEGFR-1 levels. Results: The FMS and control groups were comparable in terms of age and body mass index (p>0.05). A comparison of the serum VEGF levels of the FMS and control groups revealed a statistically insignificant difference (p>0.05), while a comparison of the serum VEGF-1 levels of the FMS and control groups revealed a statistically significant difference (p<0.05). Conclusion: Serum VEGFR-1 levels were higher in patients with FMS, while the serum VEGF levels of the FMS patients did not differ from those of the healthy controls.

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Vascular endothelial growth factor receptor-1 (VEGFR-1) signaling enhances angiogenesis in a surgical sponge model.

Cited by 17 publications

References 38 publications

<p>Effect of the Recombinant Adenovirus-Mediated HIF-1 Alpha on the Expression of VEGF in the Hypoxic Brain Microvascular Endothelial Cells of Rats</p>

<p>Effect of the Recombinant Adenovirus-Mediated HIF-1 Alpha on the Expression of VEGF in the Hypoxic Brain Microvascular Endothelial Cells of Rats</p>

Propofol attenuated TNF-α-modulated occludin expression by inhibiting Hif-1α/ VEGF/ VEGFR-2/ ERK signaling pathway in hCMEC/D3 cells

Serum Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor-1 Levels in Patients With Fibromyalgia Syndrome

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