Localization of FSHβ and its receptor in pancreas of rats
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Objective To study the localization of follicle stimulating hormone(FSH),its receptor(FSHR) and their mRNA in pancreas of rats to provide theoretic evidence for further study of FSH function in pancreas.Methods Singlestaining immunofluorescence and in situ hybridization methods were used.Results FSH protein and mRNA,and FSHR protein and mRNA immunofluorescence positive staining was localized in most of rat islet cells and partial pancreas exocrine cells,positive material distributed in the cytoplasm,not in nuclei.Conclusion Presentation of both FSH and FSHR in rat pancreas indicates that FSH may be involved in the functional regulation of pancreas through autocrine or paracrine activity.Keywords:
Follicle-stimulating hormone receptor
Immunofluorescence
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Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) have a central role in follicle growth, maturation and oestrus, but no clear pathway in the seasonal oestrus of yak (Bos grunniens) has been found. To better understand the role of FSH and LH in seasonal oestrus in the yak, six yaks were slaughtered while in oestrus, and the pineal gland, hypothalamus, pituitary gland, and gonads were collected. Using real-time PCR and immunohistochemical assays, we determined the mRNA and protein expression of the FSH and LH receptors (FSHR and LHR) in these organs. The analysis showed that the FSHR mRNA expression level was higher in the pituitary gland tissue compared with LHR (p < .01) during oestrus. By contrast, there was low expression of FSHR and LHR mRNA in the pineal gland and hypothalamus. FSHR mRNA expression was higher than that of LHR (p < .05) in the ovary, whereas LHR mRNA expression was higher than that of FSHR (p < .01) in the uterus. FSHR and LHR proteins were located in the pinealocyte, synaptic ribbon and synaptic spherules of the pineal gland and that FSH and LH interact via nerve fibres. In the hypothalamus, FSHR and LHR proteins were located in the magnocellular neurons and parvocellular neurons. FSHR and LHR proteins were localized in acidophilic cells and basophilic cells in the pituitary gland, and in surface epithelium, stromal cell and gland epithelium in the uterus. In the ovary, FSHR and LHR protein were present in the ovarian follicle. Thus, we concluded that FSHR and LHR are located in the pineal gland, hypothalamus, pituitary and gonad during oestrus in the yak. However, FSHR was mainly expressed in the pituitary gland and ovaries, whereas LHR was mainly expressed in the pituitary gland and uterus.
Follicle-stimulating hormone receptor
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Follicle-stimulating hormone receptor
Granulosa cell
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The present study was undertaken to identify the mechanisms underlying the effect of insulin-like growth factor I (IGF-I) on FSH receptor (FSHR) in rat granulosa cells. Treatment with FSH produced a substantial increase in FSHR mRNA level, as was expected, while concurrent treatment with increasing concentrations of IGF-I brought about dose-dependent increases in FSH-induced FSHR mRNA, with a maximal response 2.8-fold greater than that induced by FSH alone. IGF-I, either alone or in combination with FSH, did not affect intracellular cAMP levels, whereas it enhanced the effect of 8-bromo (Br)-cAMP on FSHR mRNA production. Taken together, these findings suggest that the ability of IGF-I to enhance FSH action concerning the induction of FSHR is exerted at sites distal to cAMP generation. We then investigated whether the effect of IGF-I and FSH on FSHR mRNA levels was the result of increased transcription and/or altered mRNA stability. The rates of FSHR mRNA gene transcription, assessed by nuclear run-on transcription assay, were not increased by the addition of IGF-I. On the other hand, the decay curves for the 2.4-kilobase (kb) FSHR mRNA transcript in primary granulosa cells significantly altered the slope of the FSHR mRNA decay curve in the presence of IGF-I and increased the half-life of the FSHR mRNA transcript. These data suggest a possible role for changes in FSHR mRNA stability in the IGF-I-induced regulation of FSHR in rat granulosa cells. Treatment with activin produced a substantial increase in FSHR mRNA level, as was expected, and concurrent treatment with IGF-I did not affect activin-induced FSHR mRNA. Our data suggest that the IGF-I effect on FSHR expression is related to cAMP production induced by FSH and may maintain FSHR mRNA level because of prolonged FSHR mRNA stability.
Follicle-stimulating hormone receptor
Gonadotropin
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Immunoperoxidase staining and radioreceptor assay were used to study the localization of LH, FSH, and PRL and their receptors in the human and rat testis. In immunohistochemical staining, the Leydig cells of both species were invariably LH positive and generally FSH negative, but there were some FSH positive cells which were morphologically indistinguishable from the Leydig cells. The tubules were LH negative. The Sertoli cells of both species, were FSH positive, whereas the spermatogonia and other germ cells were negative. Positive staining for PRL was seen in rat Leydig cells, whereas the human testes were negative. In keeping with the immunohistochemical findings, LH and FSH receptors were found in the testis of both species, but PRL receptors only in the rat. The finding of FSH positive cells in the interstitial tissue may explain why FSH increases the number of Leydig cell LH receptors and increases the sensitivity and maximum response to LH stimulation. Failure to demonstrate PRL and PRL receptors in the human testis indicates either that very low receptor concentrations are needed to bring about PRL action or that the established testicular effects of PRL are indirect.
Testicle
Gonadotropin
Immunoperoxidase
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Perinatal expression of estrogen receptor (ER) protein and mRNA and the influence of FSH on this process were examined by immunofluorescence and RT-PCR using ovaries from fetal (d 13-15 of gestation) and postnatal [postnatal d 1-15 (P1-P15)] hamsters and from 8-d-old hamsters exposed in utero to an anti-FSH serum on d 12 of gestation and saline or equine chorionic gonadotropin (eCG) on P1. A few somatic cells expressing ERalpha immunoreactivity appeared first on d 14 of gestation and increased markedly by P8-P15 in the interstitial cells and granulosa cells of primordial follicles. In contrast, appreciable ERbeta immunoreactivity was localized on d 13 of gestation, and more cells expressed ERbeta immunoreactivity by P1-P8. By P7, ERbeta immunoreactivity was present in cells adjacent to the oocytes, and by P8, ERbeta was preferentially localized in the granulosa cells. Receptor immunoreactivities decreased markedly in P8 ovaries exposed in utero to the FSH antiserum but were reversed with postnatal eCG replacement. Oocytes and somatic cells expressed ERalpha and ERbeta mRNA, and levels of ER mRNA in the ovary increased by P7-P8, corresponding to the appearance of primordial follicles. Thereafter, only ERbeta mRNA levels increased progressively with postnatal ovary development. Similar to ER protein, mRNA levels decreased significantly in FSH antiserum-treated ovaries but were restored by eCG. These results indicate that both ER subtypes are expressed in undifferentiated somatic cells and the oocytes during perinatal ovary development in the hamster; however, ERbeta expression segregates with the differentiation of granulosa cells. Furthermore, ER expression and differentiation of somatic cells to granulosa cells depend on perinatal FSH action.
Granulosa cell
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Kornyei JL, Li X, Lei ZM, Rao ChV. Restoration of human chorionic gondadotropin response in human myometrial smooth muscle cells by treatment with follicle-stimulating hormone (FSH): evidence for the presence of FSH receptors in human myometrium. Eur J Endocrinol 1996;134:225–31. ISSN 0804–4643 Human myometrial smooth muscle cells contain receptors for human chorionic gonadotropin (hCG)/ luteinizing hormone (LH). Exogenous hCG and LH can cause a modest hyperplasia in myometrial smooth muscle cells in culture. This response is lost after about the third subculture of the cells. The present study investigated whether the loss of hCG response could be restored by co-culturing with human follicle stimulating hormone (FSH). The results showed that co-culturing with FSH can indeed restore a modest mitogenic response of hCG. However, FSH alone was not mitogenic. The FSH restoration of hCG response can be blocked by antibodies to FSH or hCG but not by non-specific rabbit IgG. The FSH treatment resulted in an increase of steady state levels of hCG/LH receptor mRNA and protein in myometrial smooth muscle cells. Since the FSH actions could be receptor mediated, we investigated the presence of FSH receptor mRNA transcripts and protein in freshly dispersed myometrial smooth muscle cells. Northern blotting demonstrated that myometrial smooth muscle cells, just as rat ovary, a classical target of FSH action, contain multiple FSH receptor mRNA transcripts. Western immunoblotting demonstrated that myometrial smooth muscle cells also contain a 60 kDa FSH receptor protein just as rat ovary and human granulosa cells used as positive control tissues. The immunocytochemistry also demonstrated that myometrial smooth muscle cells, as rat ovary and human granulosa cells, contain FSH receptor immunostaining. In summary, it is novel that FSH could restore the mitogenic response of hCG in human myometrial smooth muscle cells and these cells contain FSH receptors. These findings may have functional implications for direct regulation of human myometrium not only by hCG/LH but also by FSH. ChV Rao, Department of Obstetrics and Gynecology, 438 MDR Building, University of Louisville, School of Medicine, Louisville, Kentucky 40292, USA
Myometrium
Human chorionic gonadotropin
Follicle-stimulating hormone receptor
Gonadotropin
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Follicle-stimulating hormone receptor
Gonadotropin
Granulosa cell
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Follicle-stimulating hormone receptor
Gonadotropin
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Progesterone receptor
Follicle-stimulating hormone receptor
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