This gene was found in a mouse DNA array analysis of transcripts expressed in mouse preovulatory follicles.
NCBI Summary:
Endothelin receptor type B is a G protein-coupled receptor which activates a phosphatidylinoitol-calcium second messenger system. Its ligand, endothelin, consists of a family of three potent vasoactive peptides: ET1, ET2, and ET3. Studies suggest that the multigenic disorder, Hirschsprung disease type 2, is due to mutation in endothelin receptor type B gene. A splice variant, named SVR, has been described; the sequence of the ETB-SVR receptor is identical to ETRB except for the intracellular C-terminal domain. While both splice variants bind ET1, they exhibit different responses upon binding which suggests that they may be functionally distinct.
General function
Receptor
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Cellular localization
Plasma membrane
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Ovarian function
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Expression regulated by
LH
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Ovarian localization
Granulosa, Theca, Luteal cells
Comment
Gentili M, et al.(Horm Metab Res. 2001) found that there is weak expression of ETB mRNA in luteinized human granulosa cells, compared with ETA.
A NOVEL PATHWAY INVOLVING PROGESTERONE RECEPTOR, ENDOTHELIN-2, AND ENDOTHELIN RECEPTOR B CONTROLS OVULATION IN MICE. Palanisamy GS et al. The steroid hormone progesterone (P) plays a pivotal role during ovulation. Mice lacking P receptor (Pgr) gene fail to ovulate due to a defect in follicular rupture. The P receptor (PGR)-regulated pathways that modulate ovulation, however, remain poorly understood. To identify these pathways, we performed gene expression profiling using ovaries from mice subjected to gonadotropin-induced superovulation in the presence and in the absence of CDB-2914, a synthetic PGR antagonist. Prominent among the genes that were down regulated in response to CDB-2914 was endothelin-2 (ET-2), a potent vasoactive molecule. ET-2 mRNA was transiently induced in mural granulosa cells of the preovulatory follicles immediately preceding ovulation. This induction was absent in the ovaries of PGR null mice, indicating a critical role of this receptor in ET-2 expression. To investigate the functional role of ET-2 during ovulation, we employed selective antagonists of endothelin receptors, ETR-A and ETR-B. Mice treated with an ETR-B antagonist exhibited a dramatic (>85%) decline in the number of released oocytes. Strong expression of ETR-B was observed in the mural and cumulus granulosa cells of the preovulatory follicles as well as in the capillaries lining the inner border of the theca interna. We also identified cGMP-dependent protein kinase II, a previously reported PGR-regulated gene, as a downstream target of ET-2 during ovulation. Collectively, our studies uncovered a unique pathway in which ET-2, produced by PGR in mural granulosa cells, acts in a paracrine or autocrine manner on multiple cell-types within the preovulatory follicle to control the final events leading to its rupture.
Follicle stages
Corpus luteum
Comment
Role of the Endothelin-1 System in the Luteolytic Process of Pseudopregnant Rabbits
Boiti C, et al .
The aim of this study was to better understand the role of the endothelin-1 (ET-1) system in the process controlling the corpora lutea (CL) life span in rabbits. ET-1 (10 microg iv) administration at days 9 and 12 of pseudopregnancy induced a functional luteolysis within 24 h of injection, but it was ineffective at both days 4 and 6. Pre-treatments with Bosentan, a dual ETA/ETB receptor antagonist, or cyclooxygenase (COX) inhibitor blocked the luteolytic action of ET-1, but not that induced by prostaglandin (PG) F2alpha. In CL cultured in vitro, ET-1 increased (P