Endothelin 1 overexpression 293T lysate (whole cell)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Endothelin 1 (ET-1) is a potent vasoconstrictor peptide with a molecular mass of approximately 2.5 kDa. The gene encoding ET-1 is expressed predominantly in endothelial cells where it exerts its vasoconstrictive effect. It is synthesized as a prepropeptide that undergoes cleavage to form the mature ET-1 peptide. The primary expression occurs in the vascular endothelial cells but it is also found in the kidney lung and brain indicating its widespread physiological role.

Biological function summary

ET-1 regulates vascular tonus and blood pressure. It is part of the endothelin family that includes endothelin-2 (ET-2) and endothelin-3 (ET-3). ET-1 binds to endothelin receptors such as ETA and ETB which are G protein-coupled receptors facilitating cellular signaling processes. These receptors are abundant in smooth muscle cells and the central nervous system. The interaction of ET-1 with these receptors affects not only vascular smooth muscle contraction but also cell proliferation and production of extracellular matrix proteins.

Pathways

ET-1 plays an important role in the renin-angiotensin-aldosterone system and the nitric oxide signaling pathway. ET-1 interacts closely with angiotensin II a peptide hormone that increases blood pressure by stimulating the production of endothelin in endothelial cells. The release of nitric oxide by endothelium serves as a counter-regulatory mechanism to ET-1-mediated vasoconstriction. The balance between ET-1 and nitric oxide is vital for maintaining vascular homeostasis.

ET-1 is significantly implicated in hypertension and pulmonary arterial hypertension (PAH). The overproduction of ET-1 contributes to sustained high blood pressure and arterial stiffness. In PAH ET-1 levels are increased leading to the constriction and proliferation of pulmonary vascular cells. ET-1's interaction with proteins like transforming growth factor-beta (TGF-β) further enhances its role in vascular remodeling associated with these conditions. Understanding ET-1's interaction in these pathways has made it a therapeutic target for treating these cardiovascular diseases.