Antibodies to Endothelin & Endothelin Receptors

Introduction

Endothelins (ETs) are a multifunctional large family of polypeptides. There are three well recognized members in this family (ET1, ET2, and ET3) of which ET11 appears to be the most important. They have been shown to play an important role in the pathogenesis of many life threatening diseases of humans and animals.

Endogenous ET1 is involved in a variety of conditions including systemic and pulmonary hypertension, congestive heart failure, vascular remodeling, renal failure, cancer, and cerebrovascular disease. ET1 is the principal isoform in the human cardiovascular system; it is continuously released from vascular endothelial cells by the constitutive pathway, producing intense constriction of the underlying smooth muscle and contributing to the maintenance of endogenous vascular tone. The peptide is also released from endothelial cell-specific storage granules (Weibel-Palade bodies) in response to external physiological, or perhaps pathophysiological, stimuli producing further vasoconstriction. Thus, ET1 functions as a locally released, rather than circulating, hormone, and concentrations are comparatively low in plasma and other tissues. ET2 has been less extensively studied than other ET peptides, but it is present in human cardiovascular tissues and is as potent a vasoconstrictor as ET1 in human arteries and veins.

Endothelial cells do not synthesize ET3, but the mature peptide is detectable in plasma and other tissues, including heart and brain. ET3 is unique in that it is the only endogenous isoform that distinguishes between the two endothelin receptors. It has the same affinity at the ETB receptor as ET1 but, at physiological concentrations, has little or no affinity for the ETA receptor.

Endothelin receptors are widely expressed in all tissues, contributing to the maintenance of vascular tone. In humans, ETA receptors predominate on the smooth muscle of blood vessels, and the low density of ETB receptors (<15%) also present on the smooth muscle contributes little to vasoconstriction in either normal or diseased tissue . ETB receptors are the principal type in the kidney, localizing to nonvascular tissues. Evidence is emerging that the ETB receptor functions as a "clearing receptor" to remove ET from the circulation.

Antibody Panel to Endothelin and its Receptors

Acris Antibodies offers a range of monoclonal and polyclonal antibodies to Endothelin (1,2, 3) and the endothelin receptors type A and B. The antibodies can be used for different applications such as immunoassay, Western blot and Immunohistochemistry; some of them are even suitable for Paraffin embedded sections. Antibodies SP4125P and SP4126P have been raised against Endothelin B Receptor-Like Protein 2 (ETBR-LP-2), also known as the G-Protein Coupled Receptor 37-Like 1 (GPR37L1) .

Fig.1 and Fig.2 show immunolocalization of ET1 in human bowel using antibody SM5063

Fig.3: Immunohistochemical staining of human heart Paraffin sections using antibody SP4122P to Endothelin A receptor

Fig.4: Immunohistochemical staining of Endothelin B receptor on human adrenal medulla using
antibody SP4124P

Fig.5: Immunohistochemical staining of adrenal
medulla using anti-Endothelin B receptor
antibody SP4565P

Panel to Endothelin (ET), ET receptors, and ETBR-LP-2

Endothelin (ET1, ET2, ET3), Endothelin Receptor (ETA , ETB) antibody.

Literature

Inscho EW, Imig JD, Cook AK, Pollock DM ET(A) and ET(B) receptors differentially modulate afferent and efferent arteriolar responses to endothelin. Br J Pharmacol. 2005 Oct 17;(Epub ahead of print)

Motte S, McEntee K, Naeije R. Endothelin receptor antagonists. Pharmacol Ther. 2006; 110(3) 386-414.

Davenport AP. Intern. Union of Pharmacology. XXIX. Update o Endothelin receptor nomenclature. Vol. 54(2), 219-226, June 2002.

Dupuis J, Hoeper MM. Endothelin receptor antagonists in pulmonary arterial hypertension. Eur Respir J. 2008 Feb;31(2):407-15.

Polikepahad S, Moore RM, Venugopal CS. Endothelins and airways--a short review. Res Commun Mol Pathol Pharmacol. 2006;119(1-6):3-51. Review.

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