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This Article Full Text Full Text (PDF) All Versions of this Article: 69/4/1238    most recent biolreprod.102.014753v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Inoue, K. Articles by Minegishi, T. Search for Related Content PubMed PubMed Citation Articles by Inoue, K. Articles by Minegishi, T. Agricola Articles by Inoue, K. Articles by Minegishi, T.

Mechanisms of Action of Transforming Growth Factor ß on the Expression of Follicle-Stimulating Hormone Receptor Messenger Ribonucleic Acid Levels in Rat Granulosa Cells¹

Department of Obstetrics and Gynecology,³ School of Medicine, Gunma University, Maebashi, Gunma 371-8511, Japan Department of Biochemistry,⁴ Fukui Medical University, Matsuoka, Fukui 910-1193, Japan CREST, JST (Japan Science and Technology Corporation),⁵ Saitama 322-0012, Japan

The present study was undertaken to identify the mechanisms underlying the effect of transforming growth factor (TGF) ß on FSH receptor (FSH-R) in rat granulosa cells. Compared to the control, the treatment of granulosa cells with TGFß (10 ng/ml) increased FSH-R mRNA transcripts (5.5 and 2.4 kilobases) in a time-dependent manner, with a maximum increase of approximately 2-fold at 48 h. We then investigated whether the effect of TGFß on FSH-R mRNA levels was the result of increased transcription and/or altered mRNA stability. To determine whether the FSH-R 5'-flanking region plays a role in directing FSH-R mRNA expression, the proximal area of the FSH-R 5'-flanking regions were inserted into an expression vector, pGL-Basic, which contains luciferase as the receptor gene, and the resulting plasmids were transiently transfected into rat granulosa cells. The FSH (30 ng/ml) significantly enhanced the activity of 1862 base pairs of the FSH-R 5'-flanking region, but treatment with TGFß did not significantly influence the activity induced by FSH. On the other hand, the decay curves for FSH-R mRNA transcript in primary granulosa cells showed a significant increase in half-life after the addition of TGFß. Transforming growth factor ß stimulates the expression of follistatin mRNA accumulation in a dose- and time-dependent manner. Treatment with activin produced a substantial increase in FSH-R mRNA level. Concurrent treatment with follistatin neutralized this activin effect on FSH-R mRNA, as reported, although concurrent treatment with follistatin did not affect TGFß-induced FSH-R mRNA. Therefore, the profile of the TGFß effect on FSH-R mRNA granulosa cells may be caused by the increased stability of FSH-R mRNA and insensitivity to the follistatin.

¹ Supported by a grant from the Ministry of Education, Culture, Sports, Science and Technology of Japan (13470344). M.T. was supported by Fellowships of the Japan Society for the Promotion of Science for Japanese Junior Scientists.

² Correspondence. FAX: 81 27 220 8443; tminegis{at}showa.gunma-u.ac.jp

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