Hyperoxia enhances VEGF release from A549 cells via post-transcriptional processes

Shenberger, Jeffrey S.; Zhang, Lianqin; Powell, Richard J.; Barchowsky, Aaron

doi:10.1016/j.freeradbiomed.2007.05.033

Cited by 20 publications

(15 citation statements)

References 46 publications

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“…In brain microvascular endothelial cells we demonstrate that HIF-1α stimulates both expression and secretion of VEGF. In the current study we show a significant increase in VEGF protein precedes an increase in mRNA which is consistent with studies in other cell types that document post-transcriptional regulation of VEGF levels (Shenberger et al, 2007). VEGF has been to shown to regulate HO-1 expression and activity in vascular endothelial cells.…”

Section: Discussionsupporting

confidence: 92%

Hypoxia induces angiogenic factors in brain microvascular endothelial cells

Luo

Martinez

Yin

et al. 2012

Microvascular Research

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Hypoxia is increasingly recognized as an important contributing factor to the development of brain diseases such as Alzheimer’s disease (AD). In the periphery, hypoxia is a powerful regulator of angiogenesis. However, vascular endothelial cells are remarkably heterogeneous and little is known about how brain endothelial cells respond to hypoxic challenge. The objective of this study is to characterize the effect of hypoxic challenge on the angiogenic response of cultured brain-derived microvascular endothelial cells. Brain endothelial cell cultures were initiated from isolated rat brain microvessels and subjected to hypoxia (1% O2) for various time periods. The results showed that hypoxia induced rapid (≤ 0.5 h) expression of hypoxia-inducible factor 1α (HIF-1α) and that cell viability, assessed by MTT assay, was unaffected within the first 8 h. Examination of brain endothelial cell cultures for pro- and anti-angiogenic proteins by western blot, RT-PCR and ELISA revealed that within 0.5 to 2 h of hypoxia levels of vascular endothelial growth factor and endothelin-1 mRNA and protein were elevated. The expression of heme oxygenase-1 also increased but only after 8 h of hypoxia. In contrast, similar hypoxia exposure evoked a decrease in endothelial nitric oxide synthase and thrombospondin-2 levels. Exposure of brain endothelial cell cultures to hypoxia resulted in a significant (p<0.001) decrease (94%) in tube length, an in vitro index of angiogenesis, compared to control cultures. The data indicate, despite a shift toward a pro-angiogenic phenotype, hypoxia inhibited vessel formation in brain endothelial cells. These results suggest that in brain endothelial cells expression of angiogenic factors is not sufficient for the development of new vessels. Further work is needed to determine what factors/conditions prevent hypoxia-induced angiogenic changes from culminating in the formation of new brain blood vessels and what role this may play in the pathologic changes observed in AD and other diseases characterized by cerebral hypoxia.

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Section: Discussionsupporting

confidence: 92%

Hypoxia induces angiogenic factors in brain microvascular endothelial cells

Luo

Martinez

Yin

et al. 2012

Microvascular Research

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“…Although secreted VEGF correlated with increased mRNA levels at 14 days, stents harvested at 28 days showed discordant VEGF protein and mRNA levels where secreted VEGF from select DES was found independent of transcriptional activation. The regulatory pathways of VEGF are undoubtedly complex because differential rates of healing of various DES may effect post-translational processes involving the proteolytic release of matrix-bound and receptor-bound VEGF isoforms (43). Clinical implications and perspectives.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Cell Recovery Between Comparator Polymer-Based Drug-Eluting Stents

Joner

Nakazawa

Finn

et al. 2008

Journal of the American College of Cardiology

604

405

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“…In addition, Shenberger et al. () were able to demonstrate in vitro in human lung adenocarcinoma cells and normal fibroblasts that incubation with 95% oxygen for 48 h led to a 2–3 fold increase in VEGF protein in the surrounding medium. However, VEGF‐mRNA decreased significantly in hyperoxic cells compared to normoxic controls.…”

Section: Discussionmentioning

confidence: 98%

“…Interestingly, the VEGF concentration in the epithelial lining fluid was found to increase paradoxically after hyperoxic exposure (Watkins et al 1999;Ekekezie et al 2003). In addition, Shenberger et al (2007) were able to demonstrate in vitro in human lung adenocarcinoma cells and normal fibroblasts that incubation with 95% oxygen for 48 h led to a 2-3 fold increase in VEGF protein in the surrounding medium. However, VEGF-mRNA decreased significantly in hyperoxic cells compared to normoxic controls.…”

Section: Vascular Endothelial Growth Factormentioning

confidence: 98%

Mechanical ventilation strategies alter cardiovascular biomarkers in an infant rat model

et al. 2018

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Mechanical ventilation (MV) is routinely used in pediatric general anesthesia and critical care, but may adversely affect the cardiocirculatory system. Biomarkers are increasingly measured to assess cardiovascular status and improve clinical treatment decision‐making. As the impact of mechanical ventilation strategies on cardiovascular biomarkers in ventilated infants is largely unknown, we conducted this retrospective study in a healthy in vivo infant rat ventilation model using 14‐days old Wistar rats. We hypothesized that 2 h of mechanical ventilation with high and low positive end‐expiratory pressure (PEEP), hyperoxemia, hypoxemia, hypercapnia, and hypocapnia would significantly impact B‐type natriuretic peptide (BNP), vascular endothelial growth factor (VEGF), and endothelin‐1 (ET‐1). We found BNP to be driven by both high (9 cmH2O) and low (1 cmH2O) PEEP compared to ventilated control animals (P < 0.05). VEGF concentrations were associated with high PEEP, hyperoxemia, hypoxemia, and hypocapnia (P < 0.05), whereas ET‐1 levels were changed only in response to hypoxemia (P < 0.05). In conclusion, the mode of mechanical ventilation alters plasma biomarker concentrations. Moreover, BNP and VEGF might serve as surrogate parameters for ventilation induced cardiovascular compromise and lung tissue damage. Furthermore, our data support the hypothesis, that sudden onset of hyperoxemia may trigger a quick VEGF release as a possible cellular survival reflex.

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Hyperoxia enhances VEGF release from A549 cells via post-transcriptional processes

Cited by 20 publications

References 46 publications

Hypoxia induces angiogenic factors in brain microvascular endothelial cells

Hypoxia induces angiogenic factors in brain microvascular endothelial cells

Endothelial Cell Recovery Between Comparator Polymer-Based Drug-Eluting Stents

Mechanical ventilation strategies alter cardiovascular biomarkers in an infant rat model

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