Biomedical subjects

Z M Lei

Publications and source records attributed to Z M Lei.

At least 19 recordsLinked to original sources

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↗

PubMed1996

Human chorionic gonadotropin down-regulates the expression of gonadotropin-releasing hormone receptor gene in GT1-7 neurons.

Previous studies have shown that human CG (hCG) can down-regulate the expression of GnRH gene in GT1-7 neurons and that these neurons contain GnRH receptors and a self-stimulatory mechanism in the synthesis and release of GnRH. These findings have led us to hypothesize that hCG may down-regulate GnRH receptors to disrupt the self-stimulatory mechanism. To test this hypothesis, we cultured GT1-7 neurons in the presence or absence of an optimal concentration of highly purified hCG (100 ng/ml) and then measured steady-state levels of GnRH receptor messenger RNA (mRNA) transcripts and protein. Northern blotting demonstrated that GT1-7 neurons contain a major 5.5-kb and minor 2.4-kb and 1.6-kb GnRH receptor mRNA transcripts. Ligand blotting showed that GT1-7 neurons also contain 53-kDa and 43-kDa GnRH receptor proteins. Culturing with hCG resulted in a significant decrease in steady-state levels of GnRH receptor mRNA transcripts by 12 h and GnRH receptor proteins by 6 and 12 h, followed by a return to the controls by 24 h. The treatment with hCG had no obvious effect on the transcription rate of GnRH receptor gene. The hCG treatment, however, significantly decreased the half-life of GnRH receptor mRNA transcripts from 27 h to 16 h. In summary, we conclude that treatment with hCG can down-regulate the expression of GnRH receptor gene by decreasing the stability of transcripts in GT1-7 neurons. By down-regulating GnRH receptors, hCG may disrupt the self-stimulatory mechanism in GnRH synthesis.

Cell Line, Transformed↗

PubMed1996

Up-regulation of cyclooxygenase-2 gene expression by chorionic gonadotropin during the differentiation of human endometrial stromal cells into decidua.

Human endometrial stromal cells contain human CG (hCG)/LH receptors and in vitro, hCG/LH can promote stromal cells differentiation into decidua. In the present study, we tested the hypothesis that the treatment of stromal cells with exogenous hCG/LH to promote in up-regulation of cyclooxygenase-2 (COX-2) gene expression. The stromal cells from proliferative phase endometria were cultured for 10 days with 10 ng/ml estradiol and 100 ng/ml progesterone in the presence or absence of increasing concentrations of highly purified hCG. Northern blotting demonstrated that the cells contained a 4.4-kb COX-2 messenger RNA transcript whose levels significantly increased after treatment with hCG. Western blotting showed that the cells contained a 72-kDa COX-2 protein which also significantly increased after treatment with hCG. The effect of hCG on COX-2 messenger RNA and protein was seen at 10 ng/ml and higher concentrations sustained the increased levels. Although human LH mimicked hCG, human FSH, TSH, and isolated alpha- and beta-subunits of hCG had no effect on COX-2 protein levels suggesting that the hCG effect is hormone specific and requires the conformation of native hormone. The effect of hCG on COX-2 protein paralleled the increase in media prostaglandin E2 levels indicating that the increased COX-2 gene and half-life of its transcripts to determine the molecular mechanism of hCG action. The results showed that hCG treatment had no significant effect on transcription rate of the COX-2 gene. On the other hand, treatment with hCG significantly increased the half-life of the COX-2 transcripts from 2.6 h in the control to 6.7 h after treatment. In summary, we conclude that treatment of human endometrial stromal cells with exogenous hCG to promote their differentiation into decidua results in an up-regulation of COX-2 gene expression by increasing the stability of the transcripts.

Adult↗

PubMed1996

Up-regulation of cyclooxygenase-2 gene expression by chorionic gonadotropin in mucosal cells from human fallopian tubes.

The present study investigated the regulation of cyclooxygenase-2 (COX-2) gene by human CG (hCG) in mucosal cells from human fallopian tubes. The mucosal cells contained a major [4.3 kilobase (kb)] and several minor (3.6, 2.4, and 1. 8 kb) messenger RNA (mRNA) transcripts of LH/hCG receptors and also an 80-kDa receptor protein. The receptor protein can bind 125I-hCG. Culturing mucosal cells with increasing concentrations of highly purified hCG resulted in a dose- and time-dependent increase in steady-state levels of a 4.4-kb mRNA transcript and 72-kDa protein of COX-2. Whereas hLH and hCG could mimic each other in increasing COX-2 protein levels, FSH, TSH, PRL, and isolated alpha- and beta-subunits of hCG had no effect, suggesting that the hCG effect is hormone specific and requires the conformation of native hormone. Culturing mucosal cells with increasing concentrations of hCG also resulted in a dose-dependent increase in media PGE2, levels, suggesting that the COX-2 protein increased by hCG is catalytically active. To determine the molecular mechanism of hCG action responsible for increasing the steady-state COX-2 mRNA levels, we measured the transcription rate of the COX-2 gene by nuclear run-on assay and the stability of its transcripts by an actinomycin D blocking method. The results showed that although hCG treatment had no effect on the transcription rate of COX-2 gene, it significantly increased the stability of COX-2 transcripts from 3.7 h in the control to 7.3 h after treatment. In summary, we conclude that tubal mucosal cells contain LH/hCG receptor transcripts and the receptor protein that can bind hCG. Culturing these cells with exogenous hCG and LH can up-regulate the expression of COX-2 gene by increasing the stability of transcripts. Through this up-regulation, LH and hCG may influence tubal functions that are important for early pregnancy in women.

Blotting, Northern↗

PubMed1996

cis-acting elements and trans-acting proteins in the transcription of chorionic gonadotropin/luteinizing hormone receptor gene in human choriocarcinoma cells and placenta.

We investigated the cis-acting elements and trans-acting proteins responsible for a higher basal rate of transcription of hCG/LH receptor gene in human choriocarcinoma JEG-3 cells compared with normal term pregnancy placenta. Sequential deletion of the 5'-flanking region of the gene revealed that there are three negative control regions (NCRs) designated NCR1 (-1457 to -1373 bp), NCR2 (-1051 to -835 bp), and NCR3 (-480 to -184 bp), and a promoter (-184 to -1 bp). NCR3 was more inhibitory than the other two; nearly 60-70% of the inhibitory activity resides in a sequence between -480 to -276 bp, and the rest resides in the sequence between -276 to -184 bp. Gel mobility shift assays showed that the nuclear extracts from JEG-3 cells contained proteins that form three complexes with NCR1, two with NCR2, and six with NCR3. Many of the proteins that form the complexes in NCR3 are shared with the other two NCRs. Most of the proteins that form these complexes are less abundant in nuclear extracts from JEG-3 cells than in those from placenta. The JEG-3 cell nuclear extracts also contained proteins that form three complexes with the proximal promoter of the hCG/LH receptor gene. These proteins were identified as Ap2, Ap2-like I, and Sp1 from the competition studies with synthetic excess unlabeled Ap2, Sp1, and CTF/NF1 consensus oligodeoxynucleotides and/or supershift in gel mobility assays with anti-Ap2 antibody. Although the JEG-3 cell nuclear extracts contained abundant Ap2-like protein I and low levels of Ap2 and Sp1 proteins, the placental nuclear extracts contained low levels of Ap2-like protein I and very low to nondetectable levels of Ap2 and Sp1 proteins. Deoxyribonuclease I footprinting revealed that the nuclear extracts from JEG-3 cells and placent protected the -116 to -93 bp and -65 to -45 bp regions in the proximal promoter of the hCG/LH receptor gene that contain Sp1 and Ap2 binding sites, respectively. However, the nuclear extracts from placenta only partially protected these regions, which is consistent with lower levels of proteins that bind to the proximal promoter of the gene. In summary, we conclude that the presence of low levels of proteins that bind to the NCRs and the high levels of proteins, especially Ap2-like I, that bind to the proximal promoter can potentially explain higher transcription of the hCG/LH receptor gene in JEG-3 cells compared with that in normal term pregnancy human placenta.

Adaptor Protein Complex 2↗

PubMed1996

Expression of human chorionic gonadotropin (hCG)/luteinizing hormone receptors and regulation of the cyclooxygenase-1 gene by exogenous hCG in human fetal membranes.

The present study characterized hCG/LH receptors from messenger ribonucleic acid (mRNA) to protein and whether exogenous hCG can bind and regulate the expression of the cyclooxygenase-1 (COX-1) gene in human fetal membranes from term pregnancy. Northern blotting showed that fetal membranes contain 6.0, 4.4, 2.4, and 1.4 kilobases of hCG/LH receptor mRNA transcripts. In situ hybridization revealed that amnion, chorion, and decidua contain receptor transcripts. Western immunoblotting and immunocytochemistry showed that amnion, chorion, and decidua also contain an 80-kDa receptor protein. Ligand blotting demonstrated that the 80-kDa receptor protein in fetal membranes can bind [125I]hCG, and this binding was inhibited by excess unlabeled hCG. Treatment of fetal membranes with highly purified hCG resulted in a dose- and time-dependent increase in immunoreactive COX-1 protein. The response of hCG was seen in all layers of fetal membranes. The treatment with hCG also resulted in an increase in steady state COX-1 mRNA levels. The action of hCG was prevented by cotreatment with H-89, an inhibitor of protein kinase A, but not by calphostin or lavendustin, which inhibit protein kinase C and tyrosine kinase, respectively. In summary, human fetal membranes contain hCG receptor transcripts and receptor protein that can bind hCG and up-regulate the expression of COX-1 gene.

Animals↗

PubMed1996

Novel presence of luteinizing hormone/chorionic gonadotropin receptors in human adrenal glands.

It has been well documented that a significant proportion of chronic anovulatory patients have elevated levels of dehydroepiandrosterone sulfate (DHEAS) and luteinizing hormone (LH) and normal levels of adrenocortiocotropic hormone (ACTH). We tested the hypothesis that the zones of human adrenal cortex that secrete DHEAS may contain LH/human chorionic gonadotropin (hCG) receptors. In situ hybridization showed the presence of hybridization signals representing LH/hCG receptor mRNA transcripts in the zona reticularis. Immunocytochemistry demonstrated that the zona reticularis also contained LH/hCG receptor protein. The receptor transcripts and receptor protein are also present in the deeper layer of the zona fasciculata which can also secrete DHEAS. Double immunostaining revealed that LH/hCG receptors are present in the same cells that contain cytochrome P450 side chain cleavage enzyme, suggesting that the receptor containing cells are steroidogenic. These findings may potentially explain higher DHEAS levels in chronic anovulatory women who have normal ACTH and elevated LH levels.

Adrenal Glands↗