Estradiol-17 beta, insulin-like growth factor-I, and luteinizing hormone inhibit secretion of transforming growth factor beta by rat ovarian theca-interstitial cells.
Estradiol-17 beta, insulin-like growth factor-I, and luteinizing hormone inhibit secretion of transforming growth factor beta by rat ovarian theca-interstitial cells.
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雌二醇-17β、胰岛素样生长因子-I 和黄体生成素抑制大鼠卵巢卵泡膜间质细胞分泌转化生长因子β。
DOI:
10.1095/biolreprod53.3.627
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发表时间:
1995
影响因子:
3.6
通讯作者:
Zachow,RJ
中科院分区:
文献类型:
--
作者:
Magoffin,DA;Hubert-Leslie,D;Zachow,RJ
Theca cells have been shown to secrete transforming growth factor P (TGFO3), but little is known regarding the regulation of thecal TGFj secretion. To investigate the regulation of thecal TGFP secretion and activation, rat theca-interstitial cells (TIC) isolated by Percoll gradient centrifugation were cultured with LH (0.01-10 ng/ml), androstenedione, androsterone, testosterone, or 5a-dihydrotestosterone (DHT)(all 1 x 10-9-1 x 10-M), estradiol (E2), estrone (both 1 x 10-"-1 x 10-7 M), or IGF-I (30 ng/ml). Active TGF and total TGFP in the conditioned medium were measured by bioassay. TIC spontaneously produced TGF, of which approximately 45% was in the active form. LH inhibited total TGFP secretion (45% at 0.1 ng/ml of LH) and active TGFP concentrations (40% at 0.3 ng/ml of LH). IGF-I inhibited active but not total TGF. Addition of LH did not cause any additional change in active or total TGF. Neither androstenedione, androsterone, testosterone, nor DHT had any effect on either active or total TGF3 secretion in the presence or absence of LH. In contrast, E2 inhibited both active (57%) and total (37%) TGF secretion. In the presence of LH, no additional effect of E2was observed. ICI 182 780, a pure estrogen antagonist, reversed the E2 inhibition, suggesting that the E2 effect is mediated by estrogen receptors. We next investigated the role of E2 on TGFP production by granulosa cells (GC). GC from untreated rats produced amounts of TGF similar to those produced by TIC. Approximately 50% of the total TGFP was in the active form. Treatment of the GC with FSH inhibited both total and active TGF. Treatment of the rats with diethylstilbestrol in vivo did not alter the amount of active or total TGFO produced by the GC in culture. The results of our studies are consistent with the hypothesis that GC in developing follicles can regulate the amount of androgen substrate produced by the theca cells through a combination of paracrine and autocrine mechanisms. E2 produced by GC causes a paracrine inhibition of TGFP production by TIC. This reduces the constitutive autocrine inhibition of TIC androgen production by TGF, leading to increased substrate for aromatization.
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DOI:
--
发表时间:
1994
期刊:
影响因子:
--
作者:
D. Magoffin;G. Erickson
通讯作者:
G. Erickson
影响因子:
4.8
作者:
Magoffin,DA;Weitsman,SR
通讯作者:
Weitsman,SR
DOI:
10.1210/jcem.74.2.1370508
发表时间:
1992
期刊:
The Journal of clinical endocrinology and metabolism
影响因子:
--
作者:
Mulheron,GW;Bossert,NL;Lapp,JA;Walmer,DK;Schomberg,DW
通讯作者:
Schomberg,DW
影响因子:
3.6
作者:
S. Roy;Christine Ogren;Chitrita Roy;Beth Lu
通讯作者:
Beth Lu
影响因子:
4.8
作者:
Demeter-Arlotto,M;Rainey,WE;Simpson,ER
通讯作者:
Simpson,ER