| First Author | Töhönen V | Year | 2024 |
| Journal | F S Sci | Volume | 5 |
| Issue | 4 | Pages | 306-317 |
| PubMed ID | 39168303 | Mgi Jnum | J:360824 |
| Mgi Id | MGI:7761847 | Doi | 10.1016/j.xfss.2024.08.004 |
| Citation | Tohonen V, et al. (2024) Transcriptomic profiling of the oocyte-cumulus-granulosa cell complex from estrogen receptor beta knockout mice. F S Sci |
| abstractText | OBJECTIVE: To study the role of estrogen receptor beta in follicle development and maturation and the response to gonadotropin stimulation aiming at superovulation. DESIGN: Experimental study and transcriptomic analysis. SETTING: Karolinka Institutet, medical university. ANIMAL(S): Healthy wild-type (WT) and estrogen receptor beta knockout (Esr2-KO) female mice undergoing superovulation at 4 weeks, 7 weeks, and 6 months of age. INTERVENTION(S): Not applicable. MAIN OUTCOME MEASURE(S): Oocyte yield after superovulation, transcriptomic profiling of cumulus-granulosa cell complexes and oocytes, and immunohistochemical analyses. RESULT(S): Superovulation of estrogen receptor beta (ERbeta) knockout mice resulted in reduced oocyte yield at 6 months of age compared with WT mice, but younger mice had similar yields. RNA-seq analysis of cumulus cells from superovulated WT and Esr2-KO mice identified genes and pathways associated with among others adhesion, proliferation, Wnt-signaling, and placed ERbeta in bipotential granulosa cell cluster. Loss of ERbeta increased expression of the other estrogen receptors Esr1 and Gper1. CONCLUSION(S): Our results show that ERbeta has an important role in regulating ovulation in response to exogenous gonadotropins in 6-month-old mice, but not in younger mice. Our transcriptomic and immunohistochemical observations suggest a dysregulation of the granulosa cell communication and lack of tight coordination between granulosa cell replication and antrum expansion. A significant upregulation of other estrogen receptors may support a compensatory mechanism sustaining fertility during younger age in Esr2-KO mice. |
