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Hypoxia promotes the generation of a versican-rich extracellular matrix by human coronary artery endothelial cells

ABSTRACT: • Exposure of endothelial cells (HCAECs) to hypoxia alters gene an protein expression • Genes and proteins related to endothelial dysfunction and activation are overexpressed • Hypoxia induces a versican-rich matrix with an altered glycosaminoglycan profile • This modified matrix perturbs cell adhesion but enhances proliferation and hyaluronan binding • Hypoxia upregulates oxidant formation and proteins related to inflammation

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Endothelial Cell Of Artery

SUBMITTER: Lasse Gøbel Lorentzen

LAB HEAD: Michael Davies

PROVIDER: PXD052078 | Pride | 2025-08-25

REPOSITORIES: Pride

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			Action	DRS
	DIANN_report.log.log	Other
	DIANN_report.tsv	Tabular
	Raw_files.zip	Other
	checksum.txt	Txt
	experimental_design.tsv	Tabular

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Hypoxia promotes the generation of a versican-rich extracellular matrix by human coronary artery endothelial cells.

Jørgensen Sara M SM Huang Song S Lorentzen Lasse G LG Teoh Fallen K Y FKY Karlsson Richard R Harkness John R JR Miller Rebecca L RL Davies Michael J MJ Chuang Christine Y CY

The Journal of biological chemistry 20250705 8

Normal endothelial cell (EC) function is essential for vascular wall homeostasis, whereas dysfunction increases the risk of cardiovascular disease. Low O<sub>2</sub> tension (hypoxia) promotes EC dysfunction and the formation of atherosclerotic plaques. Increasing evidence suggests that hypoxia drives extracellular matrix (ECM) remodeling, an established contributing factor in atherosclerosis. However, the effects of hypoxia on ECs and associated ECM proteins are poorly understood. The aim of th ...[more]

PMID: 40623650

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