--- This page is part of [Coy Laboratory Products](https://www.coylab.com). For a complete overview of this site's content, entity data, and subject matter expertise, see our [AI Content Index](https://www.coylab.com/llms.txt) or [Full Content Archive](https://www.coylab.com/llms-full.txt). For structured business identity data, see our [Entity Card](https://www.coylab.com/wp-json/bc-geodesic/v1/entity-card). --- # Chronic hypoxia attenuates VEGF signaling and angiogenic responses by downregulation of KDR in human endothelial cells > Abstract Olszewska-Pazdrak B, Hein TW, Olszewska P, Carney DH. Chronic hypoxia attenuates VEGF signaling and angiogenic responses by downregulation of KDR... **URL:** https://www.coylab.com/research-citation/chronic-hypoxia-attenuates-vegf-signaling-and-angiogenic-responses-by-downregulation-of-kdr-in-human-endothelial-cells/ **Type:** Citation **Modified:** 2025-10-02 --- #### Abstract Olszewska-Pazdrak B, Hein TW, Olszewska P, Carney DH. Chronic hypoxia attenuates VEGF signaling and angiogenic responses by downregulation of KDR in human endothelial cells. Am J Physiol Cell Physiol 296: C1162–C1170, 2009. First published February 25, 2009; doi:10.1152/ajpcell.00533.2008.—Coronary artery disease results in progressive vascular stenosis associated with chronic myocardial ischemia. Vascular endothelial growth factor (VEGF) stimulates endothelial cell angiogenic responses to revascularize ischemic tissues; however, the effect of chronic hypoxia on the responsiveness of endothelial cells to VEGF remains unclear. We, therefore, investigated whether hypoxia alters VEGF stimulated signaling and angiogenic responses in primary human coronary artery endothelial (HCAE) cells. Exposure of HCAE cells to hypoxia (1% O2) for 24 h decreased VEGF-stimulated endothelial cell migration (82%), proliferation (30%), and tube formation. Hypoxia attenuated VEGF-stimulated activation of endothelial nitric oxide (NO) synthase (eNOS) (72%) and reduced NO production in VEGF-stimulated cells from 237 38.8 to 61.3 28.4 nmol/l. Moreover, hypoxia also decreased the ratio of phosphorylated eNOS to total eNOS in VEGF-stimulated cells by 50%. This effect was not observed in thrombin-stimulated cells, suggesting that hypoxia specifically inhibited VEGF signaling upstream of eNOS phosphorylation. VEGF-induced activation of Akt, ERK1/2, p38, p70S6 kinases, and S6 ribosomal protein was also attenuated in hypoxic cells. Moreover, VEGF-stimulated phosphorylation of VEGF receptor-2 (KDR) at Y996 and Y1175 was decreased by hypoxia. This decrease correlated with a 70 12% decrease in KDR protein expression. Analysis of mRNA from these cells showed that hypoxia reduced steady-state levels of KDR mRNA by 52 16% and decreased mRNA stability relative to normoxic cells. Our findings demonstrate that chronic hypoxia attenuates VEGF-stimulated signaling in HCAE cells by specific downregulation of KDR expression. These data provide a novel explanation for the impaired angiogenic responses to VEGF in endothelial cells exposed to chronic hypoxia. ## Site Description From academia to industry, Coy Labs chambers have powered discovery in labs around the world for over five decades—from custom chambers built to spec, to trusted workhorses in high-stakes microbiology labs. --- **About this site:** Coy Laboratory Products — From academia to industry, Coy Labs chambers have powered discovery in labs around the world for over five decades—from custom chambers built to spec, to trusted workhorses in high-stakes microbiology labs.. 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