Biomedical subjects

Z M Lei

Publications and source records attributed to Z M Lei.

At least 19 recordsLinked to original sources

PubMed2000

HCG concentration and receptor gene expression in placental tissue from trisomy 18 and 21.

Trisomy 21 is associated with high maternal serum concentrations of intact human chorionic gonadotrophin alpha(HCG) and free beta-HCG whereas these concentrations are markedly decreased in trisomy 18. In this study, we investigated the effect of trisomy 21 and 18 on endogenous HCG concentrations and luteinizing hormone (LH)/HCG receptor expression in placental villous tissue in eight trisomy 21, six trisomy 18 and 42 chromosomally normal samples, collected at 12-16 weeks gestation. The tissue concentrations of intact HCG, free alpha-HCG and free beta-HCG subunits were measured using solid-phase two-site immunoradiometric assay. LH/HCG receptor expression was evaluated with immunohistochemistry and in-situ hybridization. Villous tissue in trisomy 21 contained higher beta-HCG concentrations than the controls (P < 0.05). In trisomy 18 cases, the beta-HCG concentration was lower than in the control group (P < 0.01). Both immunocytochemistry and in-situ hybridization demonstrated a more intense staining of the trophoblast in cases of trisomy 21 and 18, compared with controls with the strongest signal in cases of trisomy 18 (P < 0.01). We concluded that in trisomy 21 the high tissue HCG concentration and expression of LH/HCG receptor in the trophoblast may reflect the relative immaturity of the trophoblastic tissue whereas in trisomy 18, the very low concentration of endogenous HCG, associated with an over-expression of LH/HCG receptor in the trophoblast, is probably secondary to the poor differentiation of the cytotrophoblast.

Chorionic Gonadotropin, beta Subunit, Human↗

PubMed2000

Potential regulation of GnRH gene by a steroidogenic factor-1-like protein.

Steroidogenic factor-1 (SF-1) is a member of an orphan nuclear hormone receptor superfamily. It plays a critical role in the development and function of the hypothalamic-pituitary-gonadal and adrenal axis. However, whether SF-1 can regulate transcription of gonadotrophin-releasing hormone (GnRH) gene is not known. To examine this possibility, we first over-expressed SF-1 and found that it not only decreased steady state GnRH messenger ribonucleic acid (mRNA) levels but also reduced its promoter activity in GT1-7 neurons. The inhibitory effect of SF-1 was lost when the 5'-flanking region of GnRH gene containing two distal (-1479 to -1474 bp and -1059 to -1054 bp) hexamers was deleted. Gel mobility shift assays showed that GT1-7 cell nuclear extracts contained a protein that formed a specific complex with synthetic oligonucleotides containing the two distal hexamers or a consensus SF-1 binding sequence. The migration of this complex was, however, slower than the complex formed with MA-10 cell nuclear extracts which were shown to contain a 53 kDa SF-1 protein. The addition of anti-SF-1 antibody supershifted the complex formed with MA-10, but not with GT1-7 cell nuclear extracts. The same antibody, however, detected a 60 kDa protein and immunostained nuclei of GT1-7 neurons. These results are consistent with GT1-7 neurons containing an SF-1-like protein that can bind to the distal hexamer sequences in the 5'-flanking region of rat GnRH gene to inhibit its transcription.

Animals↗

PubMed1999

Treatment of human endometrial stromal cells with chorionic gonadotropin promotes their morphological and functional differentiation into decidua.

Human endometrial stromal cells contain luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors and treatment with highly purified hCG results in an up-regulation of cyclooxygenase-2 (COX-2) gene expression and increased production of prostaglandin (PG) E2. Since PGE2 promotes the differentiation of endometrial stromal cells into decidua, we tested the hypothesis that LH and hCG themselves may promote this process. The results revealed that these hormones can promote morphological as well as functional differentiation. While their action on morphological differentiation did not require the presence of estradiol (E2) and progesterone (P4), they did require them for the functional differentiation. The hCG effect was mimicked by LH, but not by follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH) or alpha and beta subunits of hCG, suggesting that the hCG action was hormone specific and requires the conformation of native hormone. The hCG treatment also increased the steady state PRL mRNA levels. This increase was due to an increase in the transcription rate of the gene rather than a decrease in the degradation of PRL transcripts. In summary, we conclude that hCG and LH can increase the morphological as well as functional differentiation of human endometrial stromal cells into decidua. This is one of the newly discovered actions of LH and hCG that may be important for the implantation of blastocyst and maintenance of pregnancy.

Adult↗

PubMed1999

Human chorionic gonadotropin exhibits potent inhibition of preterm delivery in a small animal model.

OBJECTIVE: The purpose of this study was to test the capability of human chorionic gonadotropin to inhibit prostaglandin-induced preterm delivery in a murine model. STUDY DESIGN: A preterm delivery model was developed by using intraperitoneal injection of 20 microgram of prostaglandin F(2)(alpha) to induce preterm labor in C3H/HeN inbred mice. Mice were then pretreated with human chorionic gonadotropin 4 hours before administration of prostaglandin F(2)(alpha), and time to delivery of the first pup was recorded. After initial promising results, mice were then given increasing intraperitoneal doses of human chorionic gonadotropin (100 IU, 250 IU, or 1000 IU or sodium chloride solution vehicle) 4 hours after administration of prostaglandin F(2)(alpha). The specificity of the human chorionic gonadotropin effect was assessed by treating mice with whole human chorionic gonadotropin, an equal mass dose of the beta-subunit or the alpha-subunit of human chorionic gonadotropin, or an equal mass dose of luteinizing hormone 4 hours after administration of prostaglandin F(2)(alpha). Delivery times between groups were compared by using the Mann-Whitney U test and the log-rank test. Survival estimates were computed by using the Kaplan-Meier method. RESULTS: Pilot studies in 52 mice confirmed that a single intraperitoneal injection of 20 microgram of prostaglandin F(2)(alpha) on day 16 (80% gestation) consistently induced preterm delivery compared with the effect of sodium chloride solution on control mice (prostaglandin F(2)(alpha), 19.3 +/- 2.9 hours; sodium chloride solution, 53.5 +/- 13.6 hours; P <.0001). Mice pretreated with human chorionic gonadotropin (1000 IU) demonstrated significant delays in delivery times compared with the prostaglandin-only group (prostaglandin F(2)(alpha) only, 21.9 +/- 2. 0 hours; human chorionic gonadotropin pretreatment plus prostaglandin F(2)(alpha), 48.5 +/- 20 hours; P <.0001; n = 17). Mice treated with human chorionic gonadotropin (100 IU, 250 IU, 1000 IU) 4 hours after administration of prostaglandin F(2)(alpha) demonstrated significant dose-dependent inhibition of preterm delivery compared with the prostaglandin-only group (P <.00005; n = 34). Mice treated with the alpha-subunit or the beta-subunit of human chorionic gonadotropin after prostaglandin administration did not demonstrate delays in delivery times (P =.46; n = 27). Administration of luteinizing hormone delayed delivery compared with the effect of prostaglandin F(2)(alpha) on control animals (P <.05; n = 17); however, the effect was less pronounced than that seen with a mass equivalent of human chorionic gonadotropin. CONCLUSIONS: Human chorionic gonadotropin exhibits potent inhibition of prostaglandin-induced preterm delivery in mice. The effect is dose-dependent, and whole human chorionic gonadotropin is required to elicit inhibition. Further studies are needed to determine the safety and efficacy of human chorionic gonadotropin as a potential therapy for preterm labor inhibition in human pregnancy.

Animals↗

PubMed1999

Immortalized hippocampal cells contain functional luteinizing hormone/human chorionic gonadotropin receptors.

We used immortalized HN33p cells as surrogates for hippocampal neurons to investigate the functional importance of luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors. The use of various detection techniques demonstrated that HN33p cells contain LH/hCG receptor transcripts and receptor protein that can bind 125I-hCG. Culturing them with highly purified hCG resulted in a significant, although modest, dose-and time-dependent and hormone specific increase in steady state 5-lipoxygenase (5-LO) mRNA and protein levels. The studies on signaling revealed that treatment of HN33p cells with hCG resulted in a robust dose- and a time-dependent significant increase in media cyclic AMP levels. In addition, treatment with a protein kinase (PK)A inhibitor, isoquinolinesulfonamide (H-89), but not with a PKC inhibitor, bisindolylmaleimide (Bis), prevented hCG from increasing the 5-LO protein levels. Pretreatment of HN33p cells for 48 hrs with 2 microM antisense, but not sense, phosphorothioate oligodeoxy-nucleotides (ODN) synthesized from mouse LH/hCG receptor sequence resulted in a dramatic decrease in LH/hCG receptor protein levels. In the antisense, but not in sense, ODN-treated cells, hCG was unable to increase cyclic AMP and 5-LO protein levels, suggesting that receptors are required for hCG to work in HN33p cells.

Animals↗

PubMed1999

Treatment of human endometrial gland epithelial cells with chorionic gonadotropin/luteinizing hormone increases the expression of the cyclooxygenase-2 gene.

Endometrial glands contain higher levels of LH/hCG receptors than other cells in the human uterus. The present study investigated their functional importance. Northern and Western blotting and covalent receptor cross-linking demonstrated that human endometrial gland epithelial cells in culture contained multiple LH/hCG receptor transcripts and an 80-kDa receptor protein that can bind [125I]hCG in a hormone-specific manner. Culturing cells with highly purified hCG resulted in a time- and dose-dependent increase in steady state levels of cyclooxygenase-2 (COX-2) messenger ribonucleic acid and protein and the secretion of PGE2. Although human LH could mimic hCG, FSH, TSH, and alpha- or beta-subunits of hCG had no effect on COX-2 protein levels. Studies on signaling revealed that treatment of cells with hCG resulted in an increase in cAMP levels and protein kinase A (PKA) activity. Inhibition of PKA activity by cotreatment with isoquinoline-sulfonamide (H-89) prevented hCG from increasing COX-2 protein levels. Treatment with 8-bromo-cAMP mimicked the effect of hCG, and cotreatment with a selective inhibitor of type I PKA, 8-chloro-cAMP, prevented 8-bromo-cAMP and hCG from increasing COX-2 protein levels. The requirement of receptors for LH/hCG action was investigated by 24-h treatment of human endometrial gland epithelial cells with 21-mer phosphorothioate oligodeoxynucleotides (ODNs) synthesized from human receptor sequence. Treatment with 2 micromol/L antisense, but not sense, ODN resulted in a dramatic reduction in LH/hCG receptor protein levels. hCG was unable to increase COX-2 protein, PGE2, and cAMP levels in an antisense, but not in sense, ODN-treated cells. In summary, we conclude that hCG and LH treatment can increase expression of the COX-2 gene in human endometrial gland epithelial cells. The effect was time and dose dependent, hormone specific, and mediated by the cAMP/type I protein kinase A signaling pathway. The hCG actions require a normal complement of its receptors in cells. These hCG and LH effects may be another action of these hormones in human endometrium that is important for implantation of the blastocyst and continuation of pregnancy.

Adult↗

PubMed1998

The urinary bladder of a woman is a novel site of luteinizing hormone-human chorionic gonadotropin receptor gene expression.

OBJECTIVE: The female reproductive tract contains functional luteinizing hormone-human gonadotropin receptors; therefore our objective was to test the hypothesis that bladder trigone, which is derived from intermediate mesoderm along the urogenital ridge during embryonic development of the female reproductive tract, may also contain these receptors. STUDY DESIGN: Bladder trigones or domes were biopsied from 15 premenopausal and 19 postmenopausal women undergoing surgical correction of genital prolapse, incontinence, or both. The biopsy specimens were submitted for luteinizing hormone-human chorionic gonadotropin receptor analysis by in situ hybridization and immunocytochemical examination. The receptor immunostaining was visually scored by 3 investigators without knowing the identity of the menopausal status. RESULTS: In situ hybridization demonstrated the presence of receptor transcripts, and immunocytochemical examination revealed the presence of receptor protein in bladder trigone. The bladder trigones from postmenopausal women contained lower levels compared with those from premenopausal women, implying that luteinizing hormone might down-regulate its own receptors. Transitional epithelium contained the highest receptor levels followed by smooth muscle and blood vessels. The bladder dome contained receptor levels similar to those in trigone, which suggests that a common embryologic origin is not the only reason for bladder trigone containing the luteinizing hormone-human chorionic gonadotropin receptors. Rather, they are present because luteinizing hormone-human chorionic gonadotropin may regulate bladder functions in women. CONCLUSIONS: A woman's urinary bladder, which has never been thought of as a gonadotropin target, has now been demonstrated to contain luteinizing hormone-human chorionic gonadotropin receptors. These findings suggest for the first time that gonadotropins directly regulate bladder functions in women.

Adult↗

PubMed1998

Analysis of the promoter of the luteinizing hormone/human chorionic gonadotropin receptor gene in neuroendocrine cells.

We investigated the molecular basis of luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptor gene transcription in immortalized alphaT3 gonadotropes, hypothalamic GT1-7 and hippocampal HN33p neurons. Nuclear run-on transcription, as well as transfection assays with fusion constructs of luciferase and the 5'-flanking region of LH/hCG receptor gene, revealed that GT1-7 neurons transcribe more than the alphaT3 or HN33p cells. Transient transfection of truncated reporter gene constructs and gel mobility shift assays revealed that while all neuroendocrine cells use the same promoter, they contain different levels of promoter binding proteins. Higher levels of these proteins may explain increased transcription of the LH/hCG receptor gene in GT1-7 neurons compared with alphaT3 and HN33p cells.

Animals↗

PubMed1998

Luteinizing hormone and human chorionic gonadotropin decrease type 2 5 alpha-reductase and androgen receptor protein levels in women's skin.

The present study tested the hypothesis that LH/hCG may regulate the type 2 5 alpha-reductase and androgen receptor protein levels in skin. The skin samples obtained from women undergoing abdominal laparotomy or abdominoplasty were incubated in the presence or absence of hCG. Western blotting was then performed to determine the response of type 2 5 alpha-reductase and androgen receptors. The results demonstrated that treatment with hCG resulted in a significant time- and dose-dependent, although modest, decrease in 5 alpha-reductase and androgen receptor levels compared to the controls. These effects were mimicked by LH, but not by other hormones in the glycoprotein hormone family, including alpha- and beta-subunits of hCG. Although the biological and clinical importance of this regulation remains to be determined, these findings reaffirm that human skin is among the nongonadal tissues that respond to LH and hCG treatment.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

PubMed1997

A novel regulation of the oviductal glycoprotein gene expression by luteinizing hormone in bovine tubal epithelial cells.

The hypothesis that bovine oviductal epithelial cells contain luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors and LH may regulate the oviductal glycoprotein (OGP) gene expression was tested. The results showed that bovine oviductal epithelial cells contain an 80 kDa LH/hCG receptor protein which can bind [(125)I]hCG. Culturing these cells with highly purified hCG, used as a surrogate hormone for LH, resulted in a dose and time dependent increase in a 95 kDa protein and a 2.3 kb transcript of OGP. The maximal increase of 100% was obtained with 10 ng/ml hCG and after three days of culture. LH, but not other hormones in the glycoprotein hormone family, isolated subunits of hCG, estradiol-17beta or progesterone, mimicked hCG, suggesting that the effect is hormone specific and requires the conformation of native hormone. The increase in steady state OGP mRNA levels by hCG is not due to an increase in the transcription rate of the gene. It is rather due to a significant increase in the half-life of OGP transcripts from 23 h in the control to 28 h after treatment with hCG. In summary, we conclude that LH and hCG can increase the synthesis of OGP by decreasing the degradation of its transcripts in bovine oviductal epithelial cells. Since OGP may play important roles in fertilization and growth and development of early embryo, higher LH levels present during the periovulatory period may directly participate in the early pregnancy events through increasing the synthesis of OGP.

Animals↗

PubMed1997

Novel independent and synergistic regulation of gonadotropin-alpha subunit gene by luteinizing hormone/human choriogonadotropin and gonadotropin releasing hormone in the alphaT3-1 gonadotrope cells.

The alphaT3-1 cells are immortalized anterior pituitary gonadotropes which express gonadotropin-alpha subunit gene. These cells contain receptors for gonadotropin releasing hormone (GnRH) as well as for luteinizing hormone (LH) which can also bind human choriogonadotropin (hCG). Like GnRH, LH and hCG can upregulate the expression of gonadotropin-alpha subunit gene. While 0.1-1.0 ng/ml hCG can upregulate, higher concentrations have no effect. However, these higher hCG concentrations can act in a synergistic manner with GnRH to increase the steady state mRNA and protein levels of gonadotropin-alpha subunit. The synergism between hCG and GnRH was mimicked by LH but not by other hormones in the glycoprotein hormone family or alpha or beta subunits of hCG, suggesting that the synergism is hormone specific and requires the conformation of native hormone. The hCG induced increase in gonadotropin-alpha subunit mRNA levels was due to a significant increase in the half-life of gonadotropin-alpha subunit transcripts from 7.8 +/- 1.0 h in the controls to 16.5 +/- 3.8 h after treatment with hCG. The GnRH induced increase in gonadotropin-alpha subunit mRNA levels was due to both a significant increase in the half-life to 26.2 +/- 3.0 h as well as a significant increase in the transcription rate of the gene (159.0 +/- 7.7% of the control). A greater increase in gonadotropin-alpha subunit mRNA levels following a combined treatment with GnRH and hCG was due to a further increase in half-life to 37.6 +/- 3.1 h as well as a greater increase in the transcription rate of the gene (295.1 +/- 24.2% of the control) as compared to the treatment with GnRH alone. In summary, we conclude that LH and hCG can independently and synergistically act with GnRH to increase the expression of gonadotropin-alpha subunit gene by transcriptional as well as by post-transcriptional mechanisms in alphaT3-1 cells. These effects may be important for the increase of LH levels during the preovulatory surge.

Animals↗

PubMed1997

The presence of luteinizing hormone/human chorionic gonadotropin receptors in lactating rat mammary glands.

Previous studies have implied that mammary glands might contain luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors. But no one ever previously investigated them. We now demonstrate, by using several techniques, that lactating rat mammary glands contain LH/hCG receptor mRNA transcripts and receptor protein which can bind 125I-hCG. Primarily mammary epithelial cells, and to a lesser extent the interductal stromal cells, contain the receptor transcripts and the receptor protein. These findings support the concept that mammary glands are also the targets of direct regulation by LH/hCG.

Animals↗

PubMed1997

Expression of luteinizing hormone/human chorionic gonadotropin receptor gene in benign prostatic hyperplasia and in prostate carcinoma in humans.

The findings that normal rat prostates express functional LH/hCG receptors led us to test the hypothesis that benign prostatic hyperplasia (BPH) and prostate carcinomas may also express this receptor gene. The data revealed the presence of LH/hCG receptor transcripts and receptor protein in normal and hyperplastic but not in atrophic glands present in BPH tissue. Smooth muscle and blood vessels in stroma of BPH tissue also contained receptors. Prostate carcinomas contain lower and more heterogeneous receptor levels than BPH tissue. Two human prostate cancer cell lines (LNCaP and DU 145) that were investigated showed the presence of a major 4.5-kilobase transcript and several minor transcripts and also the protein of LH/hCG receptors. However, androgen-sensitive LNCaP cells contained more receptors than androgen-insensitive DU 145 cells. In summary, we demonstrate for the first time that BPH and prostate cancer tissues and cell lines express LH/hCG receptor gene. These findings suggest that higher LH levels in aged men may play a role in BPH and/or prostate carcinomas.

Aged↗

PubMed1997

Novel expression of functional luteinizing hormone/chorionic gonadotropin receptors in cultured glial cells from neonatal rat brains.

Adult rat brains contain LH/hCG receptors, and these receptors are functional in neuroendocrine regulation and behaviors. Since glial cells are important for development, maturation, and functioning of the brain, we tested the hypothesis that these cells from neonatal rat brains may also contain functional LH/hCG receptors. Reverse-transcriptase polymerase chain reaction amplified an expected 256 base-pair LH/hCG receptor fragment from glial cells. This fragment can bind to LH/hCG receptor cDNA in Southern blotting. Northern blotting demonstrated that glial cells contain a major 2.6-kilobase (kb) and a minor 4.3-kb transcript of LH/hCG receptors. Western immunoblotting demonstrated that glial cells also contain an 80-kDa receptor protein and that its levels are significantly higher in secondary and tertiary glial cells than in primary glial cells. Immunocytochemistry confirmed that LH/hCG receptor immunostaining is present in glial cells. Since glial cells are quite active in synthesis of prostaglandins (PGs), we investigated the effect of highly purified hCG on PGD2 and PGE2 levels. The results showed that culturing secondary glial cells for three days with highly purified hCG resulted in a dose-dependent and hormone-specific increase in PGD2 and a decrease in PGE2 levels in the medium as compared to control levels. In summary, we conclude that cultured glial cells from neonatal rat brains contain functional LH/hCG receptors. Through regulation of PG synthesis, LH and hCG may influence glial cell functions that are important for neonatal brain development and function.

Animals↗

PubMed1997

Neurons from fetal rat brains contain functional luteinizing hormone/chorionic gonadotropin receptors.

Adult and neonatal rat brains contain functional LH/hCG receptors. These findings have led us to hypothesize that the fetal rat brain may also contain these receptors. To test this hypothesis, we isolated neurons from 19-day-old fetal rat brains and cultured them in chemically defined serum-free medium. The reverse transcription polymerase chain reaction amplified an expected 256-base pair size LH/hCG receptor fragment that could hybridize with a full-length LH/hCG receptor cDNA in Southern blotting. Northern blotting demonstrated that neurons contained a major 2.6 kilobase (kb) and a minor 4.3 kb transcript. Immunocytochemistry demonstrated that the neurons contained LH/hCG receptor immunostaining. Western immunoblotting showed that neurons contained an 80-kDa receptor protein that increased to a maximal level on Day 3 of culture and then gradually decreased until the 9th day of culture. Culturing neurons for 3 days in the presence of highly purified hCG resulted in a dose-dependent increase in the outgrowth of neurite processes and total cellular protein and a decrease in DNA fragmentation as compared to values in the corresponding controls. At the maximally effective hCG concentration, the number of neurite-bearing cells was increased by 53% and the total cellular protein by 60%, and DNA fragmentation decreased by 31%. In summary, this is the first study to demonstrate the presence of LH/hCG receptors and neurotrophic effects of hCG in fetal rat brain neurons. These findings imply that locally produced gonadotropins may possibly play a role in the growth and development of the fetal brain.

Animals↗

PubMed1997

Homologous down-regulation of luteinizing hormone/chorionic gonadotropin receptors by increasing the degradation of receptor transcripts in human uterine endometrial stromal cells.

We investigated the possible homologous down-regulation of LH/hCG receptors in human uterine endometrial stromal cells. The cells contained a major 4.3-kilobase (kb) and minor 3.6-kb, 2.4-kb, 1.8-kb, and 1.0-kb transcripts of receptors and an 80-kDa receptor protein that can bind [125I]hCG. Culturing these cells with increasing concentrations of highly purified hCG resulted in a dose-dependent significant decrease in steady-state levels of all the receptor transcripts, the 80-kDa receptor protein, and [125I]hCG binding as compared to the control values. The hCG effect was hormone specific and required the conformation of native hormone. The decrease in steady-state receptor transcript levels by hCG was not due to a decrease in the transcription rate of the LH/hCG receptor gene. It was rather due to a significant decrease in the half-life of receptor transcripts from 40.1 +/- 12.4 h in the control to 13.3 +/- 3.6 h after treatment. The homologous down-regulation observed in the present study may potentially explain low endometrial receptor levels in the postmenopausal human endometrium.

Adult↗

PubMed1997

Presence of functional luteinizing hormone/chorionic gonadotropin (hCG) receptors in human breast cell lines: implications supporting the premise that hCG protects women against breast cancer.

We investigated MCF-7 and MDA-MB-231 human breast cancer cell lines and immortalized mammary epithelial HBL-100 cells for the presence of functional LH/hCG receptors. The results revealed that all three breast cell lines contain LH/hCG receptor mRNA transcripts and receptor proteins that can bind 125I-hCG. The MCF-7 cells, however, contain higher levels than the others. Culturing MCF-7 cells with highly purified hCG resulted in a dose- and time-dependent significant decrease in steady-state estradiol receptor mRNA and protein levels as compared to controls, with the maximal decrease occurring after 4 h of culture with 10 ng/ml hCG. The studies on cell growth demonstrated that hCG treatment in the presence of minimal or no fetal bovine serum had a time-dependent significant inhibitory effect on MCF-7 and HBL-100, but not on MDA-MB-231 cells. In summary, our results demonstrate that human breast cell lines contain functional LH/hCG receptors. The hCG effects in MCF-7 cells are consistent with a premise that hCG protects women against breast cancer.

Blotting, Northern↗

PubMed1997

Fetal rat brains contain luteinizing hormone/human chorionic gonadotropin receptors.

The reverse transcription-polymerase chain reaction/Southern, Northern and Western blottings demonstrated that 19-day-old fetal rat brains contained the luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptor transcripts and receptor protein. Further investigation with Western blotting demonstrated that diencephalon, mesencephalon, rhombencephalon and telencephalon and several areas in each of these regions contained the LH/hCG receptor protein. The receptor protein levels in different regions were somewhat variable but they were not different from each other or from the whole brain. The 15-day-old fetal rat brains contained lower receptor protein levels which increased by 3-fold in 17-day-old and by 12-fold in 19-day-old fetal rat brains with no further significant increase in 21-day-old fetal, neonatal or adult rat brains. In summary, fetal rat brains contained LH/hCG receptors and these receptors were developmentally regulated. These findings suggest that the gonadotropins LH and hCG may regulate growth, development and differentiation in fetal brain.

Animals↗