Jul 15, 2014

Massively calcified endosomal death (MCED) of endothelial cells

BioRxiv : the Preprint Server for Biology
Larry Weisenthal

Abstract

We have discovered a novel and specific mechanism of endothelial cell death. We refer to this novel death mechanism as massively calcified endosomal death, or MCED. Exposure of endothelial cells to non-specific toxins or other physical stresses induces death by traditional apoptotic and non-apoptotic mechanisms, common to most different types of cells. In contrast, exposure of endothelial cells (but not other types of nucleated cells) to specific insults, such as oxidized pathogenic lipids (e.g. 7-ketocholesterol) or agents with known anti-angiogenic activity (e.g. bevacizumab, certain tyrosine kinase inhibitors, etc.) triggers cell death via a novel pathway, which involves the formation of massively calcified endosomes, which, in turn, escape from the dying endothelial cells as massively calcified exosomes. These endosomes/exosomes appear capable of provoking an inflammatory response, characterized by physical association of calcified microparticles with inflammatory cells (monocytes, lymphocytes, neutrophils) with resulting increased release of an inflammatory mediator (TNF) into the culture medium. Traditional media for the culture of endothelial cells are profoundly inhibitory to MCED, as are some mammalian sera and many hu...Continue Reading

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Mentioned in this Paper

Exosomes
Tumor Cells, Uncertain Whether Benign or Malignant
Biochemical Pathway
Vascular Inflammations
Tumor Necrosis Factor-alpha
Angiogenic Process
Lymphocytes as Percentage of Blood Leukocytes (Lab Test)
Pathogenic Organism
Inflammation Mediators
Toxin

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