Immunolocalisation of androgen receptor to interstitial cells in fetal rat testes and to mesenchymal and epithelial cells of associated ducts

1995 ◽  
Vol 147 (2) ◽  
pp. 285-293 ◽  
Author(s):  
G Majdic ◽  
M R Millar ◽  
P T K Saunders
Keyword(s):  
Androgen Receptor ◽  
Epithelial Cells ◽  
Leydig Cells ◽  
Interstitial Cells ◽  
Mesenchymal Cells ◽  
Wolffian Duct ◽  
Nuclear Staining ◽  
Mullerian Duct ◽  
Fetal Rat ◽  
Fetal Leydig Cells

Abstract Androgens are required for the development of male internal and external genitalia. Androgen action is mediated by an intracellular receptor which acts as a transcription factor following activation by ligand binding. The aim of the present study was to define the time of appearance of androgen receptor (AR) in the male fetal rat gonad using immunohistochemistry. Intact fetuses (days 13·5–16·5) or testicular tissue (days 16·5–20·5 and days 3–7 postnatal) were fixed in Bouins' solution and processed into paraffin wax. On day 16·5 nuclear AR were present in mesenchymal cells surrounding the Wolffian duct but those around the Mullerian duct were receptor negative. During the following day (17–18) the abundance of nuclear staining increased, becoming detectable in the epithelial cells of the Wolffian ducts. Within the testis some nuclear staining was apparent at day 17 but was confined to interstitial cells surrounding the seminiferous cords. As development of the testis proceeded the abundance of nuclear AR in peritubular and elongated mesenchymal cells increased. AR were not detected in fetal Leydig cells expressing 3β-hydroxysteroid dehydrogenase nor in the ovaries or associated ducts of female fetuses at the same ages. In conclusion, in the rat we have found AR expression detectable by immunohistochemistry in mesonephric mesenchyme to be confined to that underlying the Wolffian ducts and to be absent from the area around the degenerating Mullerian duct. On and after day 17 of gestation AR is present in Wolffian duct epithelial cell nuclei and within the testis it is confined to peritubular and interstitial cells which may have migrated from the mesonephros. Fetal Leydig cells were receptor negative. Within the seminiferous cords AR in Sertoli cells remained low until after birth and some perinuclear staining was detected in cells thought to be gonocytes. We believe this to be the first report of immunolocalisation of AR to fetal testicular interstitial cells. Journal of Endocrinology (1995) 147, 285–293

scholarly journals SIX1 cooperates with RUNX1 and SMAD4 in cell fate commitment of Müllerian duct epithelium

2018 ◽  
Author(s):  
Jumpei Terakawa ◽  
Vanida A. Serna ◽  
Devi Nair ◽  
Shigeru Sato ◽  
Kiyoshi Kawakami ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Epithelial Cells ◽  
Cell Fate ◽  
Reproductive Tract ◽  
Mesenchymal Cells ◽  
Mullerian Duct ◽  
Müllerian Duct ◽  
Duct Epithelium ◽  
Putative Precursor

AbstractDuring female mammal reproductive tract development, epithelial cells of the lower Müllerian duct are committed to become stratified squamous epithelium of vagina and ectocervix, when the expression of ΔNp63 transcription factor is induced by mesenchymal cells. The absence of ΔNp63 expression leads to adenosis, the putative precursor of vaginal adenocarcinoma. Our previous studies with genetically engineered mouse models have established that fibroblast growth factor (FGF)/mitogen-activated protein kinase (MAPK), bone morphogenetic protein (BMP)/SMAD, and activin A/runt related transcription factor 1 (RUNX1) signaling pathways are independently required for ΔNp63 expression in Müllerian duct epithelium (MDE). Here we report that sine oculis homeobox homolog 1 (SIX1) plays a critical role in the activation of ΔNp63 locus in MDE as a downstream transcription factor of mesenchymal signals. In mouse developing reproductive tract, SIX1 expression was restricted to MDE of the future cervix and vagina. SIX1 expression was totally absent in SMAD4 null MDE and was reduced in RUNX1 null and FGFR2 null MDE, indicating that SIX1 is under the control of vaginal mesenchymal factors, BMP4, activin A and FGF7/10. Furthermore, Six1, Runx1 and Smad4 gene-dose-dependently activated ΔNp63 expression in MDE within vaginal fornix. Using a mouse model of diethylstilbestrol (DES)-associated vaginal adenosis, we found DES action through epithelial estrogen receptor α (ESR1) down-regulates SIX1 and RUNX1 in MDE within the vaginal fornix. This study establishes that the vaginal/ectocervical cell fate of MDE is regulated by a collaboration of multiple transcription factors including SMAD4, SIX1 and RUNX1, and the down-regulation of these key transcription factors leads to vaginal adenosis.Author SummaryIn embryogenesis, differentiation fate of cells is specified through constant communication between neighboring cells. In this study, we investigated the molecular mechanism of epithelial cell fate commitment in the lower female reproductive organs utilizing mouse genetic models. The cell fate of epithelial cells in the uterus, cervix and vagina is directed by signaling from mesenchymal cells. We demonstrated that within the epithelial cells of the developing vagina, signals from mesenchymal cells are integrated into activities of transcription factors including SMAD4, RUNX1 and SIX1, which dose-dependently co-operate in the determination of vaginal epithelial cell fate. Disruption of these processes alters the cell fate from vaginal to uterine epithelium, resulting in a condition called vaginal adenosis, a putative precursor of vaginal adenocarcinoma. Women exposed to diethylstilbestrol (DES) in the womb have about 40 times the risk of developing vaginal adenocarcinoma. We determined that developmental exposure to DES induces vaginal adenosis by repressing SIX1 and RUNX1 through ESR1 in the epithelial cells. This discovery enhances the understanding of how early-life events, such as exposure to endocrine disruptors, causes vaginal adenosis, and thus may contribute to the prevention and therapeutic treatment of idiopathic vaginal adenocarcinoma.

Fetal rat glandular stomach epithelial cells differentiate into surface mucous cells which express cathepsin E in the absence of mesenchymal cells in primary culture

1994 ◽  
Vol 56 (1-2) ◽  
pp. 83-89 ◽  
Author(s):  
Hiroshi Fukamachi ◽  
Masao Ichinose ◽  
Satoshi Ishihama ◽  
Shinko Tsukada ◽  
Sadao Yasugi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Culture ◽  
Mesenchymal Cells ◽  
Glandular Stomach ◽  
Mucous Cells ◽  
Cathepsin E ◽  
Fetal Rat

Fetal rat glandular stomach epithelial cells differentiate into surface mucous cells which express cathepsin E in the absence of mesenchymal cells in primary culture

1994 ◽  
Vol 56 (1) ◽  
pp. 0083 ◽  
Author(s):  
Hiroshi Fukamachi ◽  
Masao Ichinose ◽  
Satoshi Ishihama ◽  
Shinko Tsukada ◽  
Sadao Yasugi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Culture ◽  
Mesenchymal Cells ◽  
Glandular Stomach ◽  
Mucous Cells ◽  
Cathepsin E ◽  
Fetal Rat

scholarly journals Growth pattern of the sex ducts in foetal mouse hermaphrodites

Development ◽  
1983 ◽  
Vol 73 (1) ◽  
pp. 59-68
Author(s):  
C. Yding Andersen ◽  
A. G. Byskov ◽  
J. Grinsted
Keyword(s):  
Epithelial Cells ◽  
Mitotic Activity ◽  
Mitotic Index ◽  
Leydig Cells ◽  
Threshold Level ◽  
Testicular Tissue ◽  
Wolffian Duct ◽  
Maximal Response ◽  
Gonadal Tissue ◽  
Normal Males

In this report the morphology of the gonads and the growth of the Wolffian and Müllerian duct in foetal mouse true hermaphrodites (16 days p.c.) have been studied and compared to that of normal mice. The ducts from the hermaphrodites were placed in one of five groups according to the proportion of male and female characteristic of the gonad. When more than 85 % of the gonadal tissue was masculine, the Wolffian ducts showed the same percentage of cells in mitosis (mitotic index, MI) as normal males. The MI of the Wolffian ducts was lower, but constant, if the gonad contained between 0 and 85 % of testicular tissue. The number of Leydig cells in the gonads showed a linear relationship with the percentage of testicular tissue. Apparently, the MI of the Wolffian duct does not increase with increasing ‘maleness’ and with the number of Leydig cells. Four possibilities are put forward to explain the constant level of MI: (1) The Leydig cells of hermaphrodites may be deficient in producing testosterone. (2) The Leydig cells may produce testosterone at a normal rate but the epithelial cells of the Wolffian duct may not respond to increasing levels of testosterone by increasing their mitotic activity. (3) The presence of female gonadal tissue may directly or indirectly inhibit the mitotic activity of the epithelial cells of the Wolffian duct. (4) The epithelial cells ofthe Wolffian duct may respond to a low threshold level of testosterone, but maximal response is only triggered by a critical higher hormone level present only in group V. In hermaphrodites, the Wolffian duct attached to a gonad without testicular tissue and withoutLeydig cells, has a MI which is significantly higher than in normal females. It is suggested thatcirculating testosterone from the contralateral gonad is responsible for this high MI. In the Müllerian duct a mitotic index similar to that of the normal females was only found when the gonad contained from 0 to 15 % of testicular tissue. If a gonad contained more than 15 % of testicular tissue, the MI of the attached Müllerian duct was much lower equalizing that of normal males. No influence on the growth of the Müllerian duct could be observed from the contralateral gonad.

444: Identification of Genes Involved in Androgen Receptor Mutant-Induced Tumorigenesis of Human Prostate Epithelial Cells

2006 ◽  
Vol 175 (4S) ◽  
pp. 144-144
Author(s):  
Xu-Bao Shi ◽  
Lingru Xue ◽  
Clifford G. Tepper ◽  
Ralph W. deVere White
Keyword(s):  
Androgen Receptor ◽  
Epithelial Cells ◽  
Human Prostate ◽  
Prostate Epithelial Cells ◽  
Receptor Mutant

Androgen receptor signalling in testicular Leydig cells is essential for Leydig cell maturation and survival

2014 ◽  
Author(s):  
Laura O'Hara ◽  
Kerry McInnes ◽  
Ioannis Simitsidellis ◽  
Steph Morgan ◽  
Laura Milne ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Maturation ◽  
Receptor Signalling

Exogenous androgens reduce the expression of INSL3, a hormone involved in normal testicular descent, in fetal Leydig cells

2014 ◽  
Author(s):  
W Colin Duncan ◽  
Fiona Connolly ◽  
Lyndsey Boswell ◽  
Graeme Burt ◽  
Alan S McNeilly ◽  
...  
Keyword(s):  
Leydig Cells ◽  
Testicular Descent ◽  
Fetal Leydig Cells

Epididymal Cyst - A Case Study

2018 ◽  
Vol 3 (4) ◽  
Author(s):  
Dr. Vinayak A. Mali ◽  
Dr.Prashanth K.
Keyword(s):  
Local Anaesthesia ◽  
Marked Improvement ◽  
Wolffian Duct ◽  
Cystic Degeneration ◽  
Mullerian Duct ◽  
Duct System ◽  
Middle Aged ◽  
Müllerian Duct ◽  
Mesonephric Duct

Cysts of the epididymis are usually congenital and derived from an embryonic remnant. These cysts are due to cystic degeneration of remnants of the paramesonephric or Mullerian duct and Remnants of the mesonephric duct or Wolffian duct system. Here we report a case of bilateral Epididymal cysts in a middle aged man with a complaint of scrotal lump and infertility since 15 years. He was treated with excision of the cysts under local anaesthesia and had a marked improvement in scrotal discomfort and urgency of micturition after the treatment.

Distinctive functioning of STARD1 in the fetal Leydig cells compared to adult Leydig and adrenal cells. Impact of Hedgehog signaling via the primary cilium.

2021 ◽  
pp. 111265
Author(s):  
Anbarasi Kothandapani ◽  
Michele Campaigne Larsen ◽  
Jinwoo Lee ◽  
Joan S. Jorgensen ◽  
Colin R. Jefcoate
Keyword(s):  
Primary Cilium ◽  
Leydig Cells ◽  
Hedgehog Signaling ◽  
Adrenal Cells ◽  
Fetal Leydig Cells
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