A Role of Insulin-Like Growth Factor I for Follicle-Stimulating Hormone Receptor Expression in Rat Granulosa Cells1

Minegishi, Takashi; Hirakawa, Takashi; Kishi, Hiroshi; Abe, Kihachiro; Abe, Yumiko; Mizutani, Tetsuya; Miyamoto, Kaoru

doi:10.1095/biolreprod62.2.325

Cited by 54 publications

(31 citation statements)

References 33 publications

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“…This suggests a role for BMP-15 in coordinating GC proliferation with FSH-dependent cytodifferentiation during follicle growth and development. Our observation that FSH stimulates the expression of FSH-R mRNA is consistent with the previous reports demonstrating that FSH itself increases FSH-R gene transcription and cell surface FSH receptors (49,50). Our results clearly demonstrated that BMP-15 completely blocks this FSH effect.…”

Section: Fig 6 Effect Of Bmp-15 On Other Fsh-induced Cellular Resposupporting

confidence: 93%

Bone Morphogenetic Protein-15 Inhibits Follicle-stimulating Hormone (FSH) Action by Suppressing FSH Receptor Expression

Otsuka

Yamamoto

Erickson

et al. 2001

Journal of Biological Chemistry

284

210

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We have recently reported that oocyte-derived bone morphogenetic protein-15 (BMP-15) can directly modulate follicle-stimulating hormone (FSH) action in rat granulosa cells. Here, we investigate underlying mechanisms of this BMP-15 effect. Treatment with BMP-15 alone exerted no significant effect on the basal expression of mRNAs encoding steroidogenic acute regulatory protein, P450 side chain cleavage enzyme, P450 aromatase, 3␤-hydroxysteroid dehydrogenase, luteinization hormone receptor, and inhibin/activin subunits. However, BMP-15 markedly inhibited the FSH-induced increases in these messages. In striking contrast, BMP-15 did not change the forskolin-induced levels of these transcripts. Thus, the inhibitory effect of BMP-15 on FSH action must be upstream of cAMP signaling. We next examined changes in FSH receptor mRNA expression. Interestingly, BMP-15 severely reduced the levels of FSH receptor mRNA in both basal and FSH-stimulated cells. To determine whether this effect was at the level of FSH function, we investigated the effect of BMP-15 on FSH bioactivity. Consistent with the mRNA data, BMP-15 inhibited the biological response of FSH, but not that of forskolin. Based on these results, we propose that BMP-15 is an important determinant of FSH action through its ability to inhibit FSH receptor expression. Because FSH plays an essential role in follicle growth and development, our findings could have new implications for understanding how oocyte growth factors contribute to folliculogenesis.

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Section: Fig 6 Effect Of Bmp-15 On Other Fsh-induced Cellular Resposupporting

confidence: 93%

Bone Morphogenetic Protein-15 Inhibits Follicle-stimulating Hormone (FSH) Action by Suppressing FSH Receptor Expression

Otsuka

Yamamoto

Erickson

et al. 2001

Journal of Biological Chemistry

284

210

View full text Add to dashboard Cite

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“…These results clearly indicated that IGF1 can in part up-regulate steroidogenic and apoptotic regulatory pathways through increasing receptor numbers for both IGF1 and FSH. In contrast, Minegishi et al (2000) reported a synergistic effect of IGF1 and FSH on FSHR expression in rat granulosa cells. Furthermore, they provided evidence that the addition of IGF1 increased the halflife of the FSHR transcript, thus providing a further mechanism by which IGF1 can affect FSH action.…”

Section: Igf1 Regulation Of Steroidogenesis and Apoptosismentioning

confidence: 88%

IGF1 induces up-regulation of steroidogenic and apoptotic regulatory genes via activation of phosphatidylinositol-dependent kinase/AKT in bovine granulosa cells

Mani¹,

Fenwick²,

Cheng³

et al. 2010

Reproduction

141

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IGF1, a potent stimulator of cellular proliferation, differentiation and development, regulates granulosa cell steroidogenesis and apoptosis during follicular development. Depending upon species and stage of follicular growth, IGF1 acts on granulosa cell steroidogenesis either alone or together with FSH. We examined the mechanism of action of IGF1 in bovine granulosa cells in serum-free culture without insulin to determine its potential role in the regulation of steroidogenic and apoptotic regulatory gene expression and to investigate the interaction of FSH with IGF1 on this mechanism. Bovine granulosa cells treated with IGF1 demonstrated a significant increase in 17b-oestradiol (OE 2 ) production, cell number and in mRNA expression of CYP11A1, HSD3B1, CYP19A1, BAX, type 1 IGF receptor (IGF1R) and FSHR, while FSH alone had no significant effects. IGF1 or FSH alone or both together had no effect on BCL2 expression. IGF1 with FSH resulted in a synergistic increase in granulosa cell number and in mRNA expression of CYP19A1 and IGF1R without altering OE 2 production. IGF1 stimulated the phosphoinositide 3 0 -OH kinase (PI3K) but not the MAPK pathway in granulosa cells, as evidenced by increased phosphorylation of AKT but not extracellularregulated kinase 1/2. Addition of the PI3K pathway inhibitor LY294002 (but not the MAPK pathway inhibitor PD98059) abrogated the increased expression of genes induced by IGF1. IGF1 therefore up-regulates the steroidogenic and apoptotic regulatory genes via activation of PI3K/AKT in bovine granulosa cells. The synergistic action of IGF1 with FSH is of likely key importance for the development of small antral follicles before selection; subsequently, other factors such as LH may also become necessary for continued cell survival.

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“…Further, this effect has been shown to occur through AP-1 activity in a PI-3 kinase and RAS/MAP kinase-dependent Table 3. 501 manner (32). IGF-I has been shown to stabilize FSH receptor mRNA (33) and LDL receptor mRNA (34), suggesting this as a potential mechanism for LPH up-regulation. Alternatively, IGF-I could potentially increase mRNA abundance by a combination of transcriptional activation and enhanced mRNA stability (34).…”

Section: Discussionmentioning

confidence: 99%

Investigation of Three Doses of Oral Insulin-like Growth Factor-I on Jejunal Lactase Phlorizin Hydrolase Activity and Gene Expression and Enterocyte Proliferation and Migration in Piglets

et al. 2000

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In a previous study, oral IGF-I at 65 nM increased lactase phlorizin hydrolase (LPH) activity and villus height in piglets, however, the mechanisms were unknown. Herein, the response to a range of doses of IGF-I was investigated and we hypothesized that LPH and villus height would respond to oral IGF-I in a dose-dependent manner. Two 14-d experiments were conducted using cesarean-derived piglets. In experiment 1, piglets (n ϭ 28) were fed formula containing 0, 33, 65, or 131 nmol/L (0, 0.25, 0.5, or 1.0 mg/L) recombinant human IGF-I. In experiment 2, 5Ј-bromodeoxyuridine was administered to piglets fed formula alone (n ϭ 4) or containing 131 nmol/L IGF-I (n ϭ 4). IGF-I did not affect body weight gain or intestinal weight or length. Jejunal villus height and LPH activity were significantly greater in piglets fed 131 nmol IGF-I/L than control piglets. Abbreviations AP-1, activator protein-1 BrdU, 5Ј-bromodeoxyuridine C/EBP, CCAAT/enhancer binding protein EF1-␣, elongation factor 1-␣ FLE, foremost labeled enterocyte HNF-1, hepatocyte nuclear factor-1 LPH, lactase phlorizin hydrolase BB LPH, brush border lactase phlorizin hydrolase proLPH h , high mannose lactase phlorizin hydrolase precursor proLPH c , complex glycosylated lactase phlorizin hydrolase precursor MAPK, mitogen activated protein kinase NHS, normal horse serum PI 3-kinase, phosphatidylinositol 3-kinaseThe presence of IGF-I in colostrum and milk (1) and IGF receptors within the intestine (2) has led to the postulate that milk-borne IGF-I could play a role in neonatal intestinal development (3). Our group and others have shown that orally administered IGF-I stimulates intestinal villus growth (4 -6) and LPH activity (E.C. 3.2.1.23-62) (6) in the neonatal piglet.However, the doses of IGF-I administered in these experiments (65-1300 nmol/L) were above the concentrations of IGF-I present in porcine colostrum (13-52 nmol/L) or mature milk (1.3-2.6 nmol/L) (7). It was unknown whether oral administration of lower doses of IGF-I would exert similar biologic effects within the neonatal intestine. Further, the mechanisms by which oral IGF-I up-regulated intestinal LPH activity and villus growth had not been described. Therefore, the goals of the current study were to determine the impact of a range of doses of oral IGF-I on intestinal villus growth and LPH activity and to investigate potential mechanisms underlying these ef-

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A Role of Insulin-Like Growth Factor I for Follicle-Stimulating Hormone Receptor Expression in Rat Granulosa Cells1

Cited by 54 publications

References 33 publications

Bone Morphogenetic Protein-15 Inhibits Follicle-stimulating Hormone (FSH) Action by Suppressing FSH Receptor Expression

Bone Morphogenetic Protein-15 Inhibits Follicle-stimulating Hormone (FSH) Action by Suppressing FSH Receptor Expression

IGF1 induces up-regulation of steroidogenic and apoptotic regulatory genes via activation of phosphatidylinositol-dependent kinase/AKT in bovine granulosa cells

Investigation of Three Doses of Oral Insulin-like Growth Factor-I on Jejunal Lactase Phlorizin Hydrolase Activity and Gene Expression and Enterocyte Proliferation and Migration in Piglets

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