Disease relevance of EDNRB

• These data suggest that endothelins stimulate ETB receptor-mediated phosphoinositide breakdown via pertussis toxin-sensitive G-protein(s), which triggers release of intracellular Ca2+, thereby activating Ca2+/calmodulin-dependent NO synthase in EC [1].

High impact information on EDNRB

• Binding studies revealed that bovine EC membrane had the binding sites of a novel agonist (BQ3020) for non-isopeptide-selective receptor subtype (ETB) [1].
• The stimulatory effect on NOx and cGMP production by ETB agonist was inhibited by NO synthase inhibitor monomethyl-L-arginine; this effect was reversed by coaddition of L-arginine, but not D-arginine [1].
• A comparison of the predicted amino acid sequence with the available bovine ETA and rat ETB endothelin receptor sequences revealed 63 and 85% homology, respectively [2].
• A cDNA clone corresponding to the entire coding region of the bovine ETB endothelin receptor mRNA was isolated from a lung cDNA library and sequenced [2].
• To probe in the isolated bovine corneal epithelium (BCE) for ET isoform and ET (i.e., ETA and ETB) receptor gene expression [3].

Biological context of EDNRB

• The amino acid sequence (Ala-Gly-X-Pro-Pro-Arg) surrounding the cleavage site (between Ala-79 and Gly-80) is conserved among the ETB endothelin receptors, explaining the above mentioned proteolytic conversion from the higher to lower Mr forms observed in various species [2].
• ETA gene expression was appreciably higher in the basal cells than in the suprabasal cells, whereas the pattern for ETB was reversed [4].
• Physical mapping of the endothelin receptor type B to bovine chromosome 12 [5].
• RES-1149-1 and -2 selectively inhibited the ET-1 binding to endothelin type B receptor (ETB receptor) with IC50 values of 1.5 microM and 20 microM, respectively [6].
• The endothelin receptor type B (ETR-B) mRNA expression increased during late luteal phase and further after regression [7].

Anatomical context of EDNRB

• Characterization of endothelin A (ETA) and endothelin B (ETB) receptors in cultured bovine retinal pericytes [8].
• ETB and epidermal growth factor receptor stimulation of wound closure in bovine corneal epithelial cells [4].
• Delphinidin-3-rutinoside relaxes the bovine ciliary smooth muscle through activation of ETB receptor and NO/cGMP pathway [9].
• Endothelium localization of ETB receptor revealed by immunohistochemistry [10].
• The ETB receptor has been found to be predominantly expressed in the vascular endothelium of various bovine tissues by immunostaining with a highly specific antiserum that does not cross-react with ETA [10].

Associations of EDNRB with chemical compounds

• The increased transcription can be attributed to ETB receptor blockade, because BQ-788, but not BQ-123, increased PPE-1 transcription [11].
• Bosentan, a dual ETA/B receptor antagonist, and BQ788 (ETB receptor antagonist) treatment resulted in a 1.6-fold and 1.3-fold increase, respectively in luciferase activity as compared with the untreated control [11].
• After treatment with 10(-7) M alltrans retinoic acid (an inducer of differentiation), 10(-6) M sarafotoxin (S-6-c) (a selective ETB agonist), had a similar effect [3].
• ET-1 inhibition of histamine-induced [(3)H]cyclic AMP was reversed by the ET-A receptor antagonist BQ-123 while the ET-B receptor antagonist BQ-788 had no effect [12].
• These data suggest that endothelial ETB receptors are functionally coupled to adenylate cyclase, possibly via Gi protein [13].

Analytical, diagnostic and therapeutic context of EDNRB

• Northern blot analysis demonstrated the expression of mRNA for ETB receptor [1].
• The C-terminal hexapeptide ET-1[16-21], which has been reported as an ETB receptor agonist but which gave no reactivity in the ELISA, also was investigated [14].
• Affinity cross-linking of the receptors showed two distinct protein bands on SDS-PAGE of 66 and 45 kd, corresponding to ETA and ETB [8].
• In situ hybridization histochemistry was used to characterize ETA and ETB gene expression in the BCE [4].

References