High impact information on EDNRA

• 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 [1].
• Activation of ETA and PDGF receptors was associated with differential stimulation of thymidine incorporation; ET-1 induced a low-amplitude bell-shaped dose-response curve; PDGF induced a sustained sigmoidal and dose-dependent rise [2].
• Pericytes expressed BQ-123-sensitive ETA receptors for endothelins as evidenced by 125I-Et-1 binding experiments [3].
• The present study was designed to characterize ETA receptor gene expression in different ovarian cell types and its hormonal regulation [4].
• At this latter stage, high ETA receptor expression concurred with low prostaglandin F2alpha receptor mRNA [4].

Biological context of EDNRA

• ETA receptor messenger RNA (mRNA) levels were high in follicular cells as well as in CL during luteal regression [4].
• Our findings may therefore suggest that, during early stages of luteinization when peak levels of both LH and insulin-like growth factor I exist, the expression of ETA receptors in the gland are suppressed [4].
• RES-1214-1 and -2 selectivity inhibited the ET-1 binding to endothelin type A receptor (ETA receptor) with IC50 values of 1.5 microM and 10 microM, respectively [5].
• ET-1 inhibited progesterone production by luteal cells in a dose-dependent manner via selective ET-1 binding sites (ETA) [6].

Anatomical context of EDNRA

• Among these various cell populations, the highest ETA receptor mRNA levels were found in endothelial cells. cAMP elevating agents, forskolin and LH, suppressed ETA receptor mRNA expression in luteinized theca cells (LTC) [4].
• To probe in the isolated bovine corneal epithelium (BCE) for ET isoform and ET (i.e., ETA and ETB) receptor gene expression [7].
• The ETA receptor gene was expressed by all three major cell populations of the bovine CL; i.e. small and large luteal cells, as well as in luteal endothelial cells [4].
• In luteinized granulosa cells (LGC), 10 and 100 ng/ml of insulin-like growth factor I and insulin (only at a concentration of 2000 ng/ml) markedly decreased ETA receptor mRNA levels [4].
• 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 [8].

Associations of EDNRA with chemical compounds

• 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 [9].
• The peptide is produced within the gland where it inhibits progesterone production by acting via the selective type A endothelin (ETA) receptors [4].
• We isolated endothelin receptor A (ETA) from bovine lungs in a single-step purification procedure using antibodies raised against synthetic peptides that correspond to extra- and intracellular domains of the rat bradykinin receptor [10].
• 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 [11].

Analytical, diagnostic and therapeutic context of EDNRA

• Affinity cross-linking of the receptors showed two distinct protein bands on SDS-PAGE of 66 and 45 kd, corresponding to ETA and ETB [12].
• In situ hybridization histochemistry was used to characterize ETA and ETB gene expression in the BCE [13].
• ETA receptor mRNA and protein expression was assessed by real time RT-PCR and western blotting, respectively [14].

References