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Calciprotein particle-activated endothelial cells aggravate smooth muscle cell calcification via paracrine signalling

ABSTRACT: Chronic kidney disease (CKD) is associated with increased cardiovascular risk, morphologically characterized by vascular calcification (VC). In CKD, high serum phosphate levels result in enhanced calcification propensity and the formation of circulating crystalline nanoaggregates (calciprotein particles, CPP2) containing calcium, phosphate and serum proteins. CPP2 can induce VC directly and this is recapitulated in vascular smooth muscle cells (VSMCs) in vitro. Under physiological conditions, vascular endothelial cells (ECs), rather than VSMCs are primarily exposed to circulating CPP2. Knowledge on the modulating effects of ECs on VC development is still in its infancy. The aim of this study was to investigate the paracrine signaling between ECs and VSMCs in CPP2-induced VC. To identify secreted soluble factors for CPP2-activated ECsthis factor, CPP2-activated ECs secretome was analyzed using mass spectrometry (LC/MS).

ORGANISM(S): Homo Sapiens

SUBMITTER: Jan-Luuk Hillebrands

PROVIDER: PXD047477 | iProX | Thu Nov 30 00:00:00 GMT 2023

REPOSITORIES: iProX

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