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Thresholds of Endoglin Expression in Endothelial Cells Explains Vascular Etiology in Hereditary Hemorrhagic Telangiectasia Type 1. | LitMetric

AI Article Synopsis

  • Hereditary Hemorrhagic Telangiectasia type 1 (HHT1) is a genetic disorder marked by abnormal connections between arteries and veins, leading to bleeding, caused by mutations in a specific receptor gene.
  • Researchers found that low levels of the endoglin protein in blood vessels are linked to the severity of symptoms across various organs, with the skin showing the lowest levels, indicating an early site for vascular issues.
  • The study suggests that there is a critical threshold of endoglin necessary for healthy blood vessel function, and enhancing endoglin expression through potential drugs might offer protection against the disease's harmful effects.

Article Abstract

Hereditary Hemorrhagic Telangiectasia type 1 (HHT1) is an autosomal dominant inherited disease characterized by arteriovenous malformations and hemorrhage. HHT1 is caused by mutations in , which encodes an ancillary receptor for Transforming Growth Factor-β/Bone Morphogenetic Protein-9 expressed in all vascular endothelial cells. Haploinsufficiency is widely accepted as the underlying mechanism for HHT1. However, it remains intriguing that only some, but not all, vascular beds are affected, as these causal gene mutations are present in vasculature throughout the body. Here, we have examined the endoglin expression levels in the blood vessels of multiple organs in mice and in humans. We found a positive correlation between low basal levels of endoglin and the general prevalence of clinical manifestations in selected organs. Endoglin was found to be particularly low in the skin, the earliest site of vascular lesions in HHT1, and even undetectable in the arteries and capillaries of heterozygous endoglin mice. Endoglin levels did not appear to be associated with organ-specific vascular functions. Instead, our data revealed a critical endoglin threshold compatible with the haploinsufficiency model, below which endothelial cells independent of their tissue of origin exhibited abnormal responses to Vascular Endothelial Growth Factor. Our results support the development of drugs promoting endoglin expression as potentially protective.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396348PMC
http://dx.doi.org/10.3390/ijms22168948DOI Listing

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