Journal article

High intraluminal pressure promotes vascular inflammation via caveolin-1

DL Michell, WA Shihata, KL Andrews, NAZ Abidin, AM Jefferis, AK Sampson, NG Lumsden, O Huet, MO Parat, GL Jennings, RG Parton, KJ Woollard, DM Kaye, JPF Chin-Dusting, AJ Murphy

Scientific Reports | Published : 2021

Abstract

The aetiology and progression of hypertension involves various endogenous systems, such as the renin angiotensin system, the sympathetic nervous system, and endothelial dysfunction. Recent data suggest that vascular inflammation may also play a key role in the pathogenesis of hypertension. This study sought to determine whether high intraluminal pressure results in vascular inflammation. Leukocyte adhesion was assessed in rat carotid arteries exposed to 1 h of high intraluminal pressure. The effect of intraluminal pressure on signaling mechanisms including reactive oxygen species production (ROS), arginase expression, and NFĸB translocation was monitored. 1 h exposure to high intraluminal pr..

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University of Melbourne Researchers

Grants

Awarded by State Government of Victoria


Funding Acknowledgements

This study was supported by a National Health and Medical Research Council of Australia program grant NHMRC#1036352 (JCD) and postgraduate scholarship NHMRC#1017847 (DLM) and supported in part by the Victorian Government's Operational Infrastructure Support Program. RGP is supported by grants and a fellowship from the National Health and Medical Research Council of Australia (grants APP1140064 and APP1150083 and fellowship APP1156489). AJM is supported by a CSL Centenary Award.