Abstract
Endothelins are powerful vasoconstrictor peptides that play numerous other roles. Endothelin-1 (ET1) is the principal isoform produced by the endothelium in the human cardiovascular system. Endothelin-3 (ET3) and its rPptor affinity have been demonstrated to support neuronal repair mechanisms throughout life. In multiple sclerosis (MS), the role of vasoactive peptides are not well defined. Here we focus on ET3, specifically the plasma levels between MS patients and healthy subjects. Furthermore, we evaluated the changes in ET1 and ET3 plasma levels during different disease phases, the correlation between ET3 and cerebral circulation time, and the relationship between ET1 and ET3. In MS patients, the ET3 plasma levels were altered in a time-dependent manner. These results could support a putative role of ET3 in neuroprotection and/or neuroimmune modulation over time.
Highlights
Endothelin peptides (ETs) comprise of three structurally similar 21-amino acid vasoactive peptides
The biosynthetic pathway of ETs is considered to be similar: 1. a large precursor designated preproET is formed; 2. after enzymatic removal of a signal peptide, proET is cleaved by a protease leading to the formation of big ET, 3. big ET is hydrolyzed into the small, mature ET1 by an endothelin-converting enzyme (ECE)
The mammalian ECE family consists of three known forms (ECE-1, ECE-2, ECE-3), which are classified into the neutral endopeptidase group of proteins [6]
Summary
Endothelin peptides (ETs) comprise of three structurally similar 21-amino acid vasoactive peptides. The mammalian ECE family consists of three known forms (ECE-1, ECE-2, ECE-3), which are classified into the neutral endopeptidase group of proteins [6]. Each member of this family shows homology to the others, mainly in the C-terminal part of the sequence that is responsible for catalytic activity. One possible source of circulating big ET3 could be the adrenal gland [2] This peptide has been visualized in secretory cells of the medulla using selective antisera, mature ET3 could not be detected [9,10]. Changes associated with the disease have not been extensively investigated, but concentrations of ET3 increased significantly in hemodialysis patients
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