Sertoli cells proliferate in adult rats with prenatal exposure to 3,3′,4,4′,5-pentachlorobiphenyl

2011 ◽  
Vol 86 (1) ◽  
pp. 159-162 ◽  
Author(s):  
Shin Wakui ◽  
Tomoko Muto ◽  
Yoshihiko Suzuki ◽  
Hiroyuki Takahashi ◽  
Hiroshi Hano
2021 ◽  
Vol 219 ◽  
pp. 112323
Author(s):  
Xiang Zhou ◽  
Tongtong Zhang ◽  
Lebin Song ◽  
Yichun Wang ◽  
Qijie Zhang ◽  
...  

1994 ◽  
Vol 116 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Charles J. Heyser ◽  
Lavanya Rajachandran ◽  
Norman E. Spear ◽  
Linda Patia Spear
Keyword(s):  

2020 ◽  
Vol 212 ◽  
pp. 108008 ◽  
Author(s):  
Mette Kongstorp ◽  
Inger Lise Bogen ◽  
Tom Stiris ◽  
Jannike Mørch Andersen

2015 ◽  
Vol 227 (2) ◽  
pp. 117-127 ◽  
Author(s):  
P Nguyen ◽  
S Khurana ◽  
H Peltsch ◽  
J Grandbois ◽  
J Eibl ◽  
...  

Prenatal exposure to glucocorticoids (GCs) programs for hypertension later in life. The aim of the current study was to examine the impact of prenatal GC exposure on the postnatal regulation of the gene encoding for phenylethanolamineN-methyltransferase (PNMT), the enzyme involved in the biosynthesis of the catecholamine, epinephrine. PNMT has been linked to hypertension and is elevated in animal models of hypertension. Male offspring of Wistar-Kyoto dams treated with dexamethasone (DEX) developed elevated systolic, diastolic and mean arterial blood pressure compared to saline-treated controls. Plasma epinephrine levels were also elevated in adult rats exposed to DEXin utero. RT-PCR analysis revealed adrenal PNMT mRNA was higher in DEX exposed adult rats. This was associated with increased mRNA levels of transcriptional regulators of the PNMT gene: Egr-1, AP-2, and GR. Western blot analyses showed increased expression of PNMT protein, along with increased Egr-1 and GR in adult rats exposed to DEXin utero. Furthermore, gel mobility shift assays showed increased binding of Egr-1 and GR to DNA. These results suggest that increased PNMT gene expression via altered transcriptional activity is a possible mechanism by which prenatal exposure to elevated levels of GCs may program for hypertension later in life.


1995 ◽  
Vol 109 (4) ◽  
pp. 734-743 ◽  
Author(s):  
Charles J. Heyser ◽  
Norman E. Spear ◽  
Linda Patia Spear

2004 ◽  
Vol 183 (1) ◽  
pp. 79-90 ◽  
Author(s):  
A Bozec ◽  
F Chuzel ◽  
S Chater ◽  
C Paulin ◽  
R Bars ◽  
...  

In utero exposure to exogenous anti-androgenic compounds induces a wide range of abnormalities of the reproductive system, including hypospermatogenesis, cryptorchidism and hypospadias. By using rats exposed in utero to the anti-androgenic compound flutamide (0.4, 2 or 10 mg/kg per day), it has been shown that hypospermatogenesis in adult testes could be related to (i) a long-term apoptosis in germ cells but not in somatic Leydig and Sertoli cells as evidenced by the TUNEL approach and (ii) alterations in the mRNA and protein expression of pro- (Bax, Bak, Bid) and anti-apoptotic (Bcl-2, Bcl-w) members of the Bcl-2 family. Indeed, the number of apoptotic germ cells increased with the dose of flutamide administered and the apoptotic germ cells were mainly detected at androgen-dependent stages VII–VIII. Moreover, for the Bcl-2-related proteins that were expressed mainly in the germ cells, a decrease in the levels of anti-apoptotic peptides Bcl-w (60%, P=0.003) and Bcl-2 (90%, P=0.0001) was observed at 2 mg/kg per day flutamide and an increase in levels of the pro-apoptotic Bax (2.3-fold, P=0.0004) was detected at 10 mg/kg per day. In contrast, the levels of pro-apoptotic peptide Bak that was mainly expressed in somatic cells decreased (70%, P=0.0008) at 10 mg/kg per day. Such alterations in Bcl-2-related peptides occurred mainly at the protein level except for Bcl-2 (72%, P=0.0001) and Bak (43%, P=00002) transcripts. Together, these results showed that the apoptosis observed in adult germ cells from rats exposed in utero to flutamide may result from a long-term alteration in the balance between pro- and anti-apoptotic Bcl-2-related molecules in favour of pro-apoptotic proteins. These data further supported the concept of an androgen-dependent fetal programming that is in relation with an alteration of the expression of Bcl-2-related genes/proteins promoting apoptosis in testicular germ cells of adult rats with fetal androgen disruption.


2011 ◽  
Vol 36 (5) ◽  
pp. 1114-1125 ◽  
Author(s):  
Tomasz Schneider ◽  
Nicholas Ilott ◽  
Giovana Brolese ◽  
Lisiane Bizarro ◽  
Philip J E Asherson ◽  
...  

1987 ◽  
Vol 114 (3) ◽  
pp. 459-467 ◽  
Author(s):  
V. Papadopoulos ◽  
P. Kamtchouing ◽  
M. A. Drosdowsky ◽  
M. T. Hochereau de Reviers ◽  
S. Carreau

ABSTRACT Production of testosterone and oestradiol-17β by Leydig cells from adult rats was stimulated by LH or dibutyryl cyclic AMP (10 and 2·5-fold respectively). The addition of spent medium from normal, hemicastrated or γ-irradiated rat seminiferous tubule cultures, as well as from Sertoli cell cultures, to purified Leydig cells further enhanced both basal (44 and 53% for testosterone and oestradiol-17β respectively) and LH-stimulated (56 and 18%) steroid output. Simultaneously, a decrease (20–30%) in intracellular cyclic AMP levels was observed. This stimulating factor (or factors) secreted by the Sertoli cells is different from LHRH, is of proteinic nature and has a molecular weight ranging between 10 000 and 50 000; its synthesis is not controlled by FSH nor by testosterone. This factor(s) involved in rat Leydig cell steroidogenesis, at a step beyond the adenylate cyclase, does not require protein synthesis for testosterone formation whereas it does for oestradiol-17β production. It should be noted that a germ cell–Sertoli cell interaction modulates the synthesis of this factor(s). J. Endocr. (1987) 114, 459–467


1985 ◽  
Vol 89 (3) ◽  
pp. 583-591 ◽  
Author(s):  
Daniel D. Savage ◽  
Edward Reyes
Keyword(s):  

2019 ◽  
Vol 20 (1) ◽  
pp. 184 ◽  
Author(s):  
Akio Horibe ◽  
Nabil Eid ◽  
Yuko Ito ◽  
Yoshinori Otsuki ◽  
Yoichi Kondo

In a recent study, we reported that acute ethanol exposure enhanced autophagy in Sertoli cells (SCs) of adult rats. However, further research is needed to clarify the specific spermatogenic stage exhibiting the highest autophagic response, the mechanisms behind such specificity, and the related relevance to sperm. This brief report provides results indicating that stages VII–VIII (androgen-dependent or spermiation stages) of the spermatogenic cycle exhibited more marked autophagic response in acute-ethanol treated rats (ETRs) than other stages based on suppression of androgen receptor (AR), analysis of microtubule-associated protein 1 light chain 3 (LC3) (an autophagosomal marker) immunostaining in SCs, double labeling of LC3 and lysosomal proteins and electron microscopy. Ultrastructural observations and TUNEL method revealed a notable presence of phagocytosed apoptotic germ cells and retained sperm in SCs of ETRs at these specific stages—a finding rarely observed in control testes. In addition, PTEN-induced putative kinase 1 ( PINK1) (a sensor of mitochondrial damage and mitophagy) and giant lipid droplets were found to have accumulated in SCs of ETRs at same stages. Our data show novel findings indicating that stages VII–VIII of the spermatogenic cycle exhibit high levels of autophagy, specifically under stress conditions, as expressed by the term autophagic stages. This stage-specific upregulation of autophagy in SCs may be related to AR suppression, mitochondrial damage, lipid accumulation, and phagocytosis of apoptotic cells. The phenomenon may be an essential part of ensuring the viability of SCs and supporting germ cells in toxic environments.


Sign in / Sign up

Export Citation Format

Share Document