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Articles by K. S. Korach
Total Records ( 2 ) for K. S. Korach
  B. J Deroo , K. F Rodriguez , J. F Couse , K. J Hamilton , J. B Collins , S. F Grissom and K. S. Korach
 

Granulosa cells of preovulatory follicles differentiate in response to FSH, and this differentiation is augmented by estradiol. We have previously shown that FSH-mediated granulosa cell differentiation requires functional estrogen receptor-β (ERβ) by demonstrating that the granulosa cells of ERβ–/– FSH-treated mice are unable to maximally induce expression of the LH receptor (an indicator of granulosa cell differentiation) compared with ERβ+/+ controls. As a result, FSH-primed ERβ–/– granulosa cells exhibit a reduced response to a subsequent ovulatory dose of LH. In this study, we further characterized the attenuated response of ERβ–/– granulosa cells to stimulation by LH and FSH using isolated mouse granulosa cells and primary granulosa cell cultures. We observed a 50% reduction in cAMP levels in cultured ERβ–/– granulosa cells exposed to LH compared with ERβ+/+ controls. We also observed an attenuated genomic response in granulosa cells isolated from FSH-primed ERβ–/– mice compared with ERβ+/+ controls. Our data indicate that this attenuated response may result from inadequate levels of cAMP, because cAMP levels in cultured ERβ–/– granulosa cells exposed to forskolin were approximately 50% lower than in ERβ+/+ granulosa cells. Phosphorylation of cAMP regulatory element binding protein, an indicator of protein kinase A activity, was also reduced in FSH-treated ERβ–/– granulosa cells compared with ERβ+/+ controls. These are the first data to indicate that ERβ plays a role in the induction of the cAMP pathway in mouse granulosa cells and that disruption of proper ERβ signaling associated with this pathway may cause negative effects on ovulation and fertility.

  S. C Hewitt , J. E O'Brien , J. L Jameson , G. E Kissling and K. S. Korach
 

In vitro models have been used to demonstrate that estrogen receptors (ERs) can regulate estrogen-responsive genes either by directly interacting with estrogen-responsive element (ERE) DNA motifs or by interacting with other transcription factors such as AP1. In this study, we evaluated estrogen (E2)-dependent uterine gene profiles by microarray in the KIKO mouse, an in vivo knock-in mouse model that lacks the DNA-binding function of ER and is consequently restricted to non-ERE-mediated responses. The 2- or 24-h E2-mediated uterine gene responses were distinct in wild-type (WT), KIKO, and ERKO genotypes, indicating that unique sets of genes are regulated by ERE and non-ERE pathways. After 2 h E2 treatment, 38% of the WT transcripts were also regulated in the KIKO, demonstrating that the tethered mechanism does operate in this in vivo model. Surprisingly, 1438 E2-regulated transcripts were unique in the KIKO mouse and were not seen in either WT or ERKO. Pathway analyses revealed that some canonical pathways, such as the Jak/Stat pathway, were affected in a similar manner by E2 in WT and KIKO. In other cases, however, the WT and KIKO differed. One example is the Wnt/β-catenin pathway; this pathway was impacted, but different members of the pathway were regulated by E2 or were regulated in a different manner, consistent with differences in biological responses. In summary, this study provides a comprehensive analysis of uterine genes regulated by E2 via ERE and non-ERE pathways.

 
 
 
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