Localization of the glucocorticoid receptor in testis and accessory sexual organs of male rat

Schultz, Rüdiger; Isola, Jorma; Parvinen, Martti; Honkaniemi, Jari; Wikström, Ann Charlotte; Gustafsson, Jan‐Åke; Pelto‐Huikko, Markku

doi:10.1016/0303-7207(93)90036-j

Cited by 94 publications

(61 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…spermatogonia, of the testis. Glucocorticoid receptors were detected in the nuclei of spermatocytes of rats (Schultz et al, 1993). Direct immunofluorescence in this study, however, did not reveal intense fluorescence in the spermatocyte nuclei of rats injected with hydrocortisone-BSA or corticosterone-BSA.…”

Section: Discussioncontrasting

confidence: 85%

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Nishimura

Nakano

2000

Cell Struct. Funct.

View full text Add to dashboard Cite

ABSTRACT. Through observations of colloidal gold with silver enhancement, we have demonstrated that 2-nm colloidal gold labeled-testosterone-bovine serum albumin (BSA) conjugate or hydrocortisone-BSA conjugate injected intravenously enters the hormone-target cell nuclei of rats (Nishimura and Ichihara, 1997; Nakano, 1997, 1999). To confirm immunocytochemically whether the nature of BSA in the steroid hormone-BSA conjugates (steroid-BSAs) remains intact in the hormone-target cell nuclei, testosterone-BSA, hydrocortisone-BSA or corticosterone-BSA was injected into the vascular system of rats, then the liver and testes of rats killed 2 h postinjection were reacted with FITC-conjugated anti-BSA antibody, and examined under fluorescence microscopy and confocal laser scanning microscopy. In the liver of rat injected with testosterone-BSA, the fluorescence was observed in the nuclei of endothelial cells, but not in the nuclei of hepatocytes, hepatic stellate cells and Kupffer cells. In the liver of rat injected with hydrocortisone-BSA, intense fluorescence was seen in the nuclei of hepatic stellate cells, but did not seem to be present in the nuclei of the other three kinds of cells. In the liver of rat injected with corticosterone-BSA, the fluorescence seemed to be in a few nuclei of hepatic stellate cells, and appeared as speckles in a few nuclei of the hepatocytes and Kupffer cells. In some seminiferous tubules of rat injected with testosterone-BSA, fluorescence was observed in the nuclei of spermatocytes and spermatids. These results suggest that BSA conjugated with steroid hormone can enter the hormone-target cell nuclei with its antigenicity kept intact, and that the fate of steroid-BSAs is decided at the cell membrane level.Key words: testosterone-BSA/hydrocortisone-BSA/corticosterone-BSA/target cell nuclei/ in vivo/immunocytochemistry Steroid hormones circulate in blood plasma in three physical states: free, albumin-bound, and bound to serum steroid binding proteins such as sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) (Kuhn,

show abstract

Section: Discussioncontrasting

confidence: 85%

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Nishimura

Nakano

2000

Cell Struct. Funct.

View full text Add to dashboard Cite

show abstract

“…It appears that the number of apoptotic Leydig cells observed were not sufficient to cause a decrease in the level of testosterone after acute stress induction. As above, germ cell apoptosis might also be induced by corticosterone, since glucocorticoid receptors (GR) have been identified in the cytoplasm of primary spermatocytes [Schultz et al 1993]. Therefore, corticosterone may be inhibiting, through a Figure 7.…”

Section: Discussionmentioning

confidence: 96%

“…A decrease in the level of testosterone affects conversion of round spermatids during spermiogenesis at stages 7 to 8 causing premature detachment that prevents elongation [O'Donnell et al 1996;Sofikitis et al 1999], thereby decreasing daily sperm production which may reflect our previous observation of decreased testosterone. Conversely, stress-induced corticosterone release might affect the epididymal microenvironment through the epithelial cytoplasmic and nuclear glucocorticoid receptor [Schultz et al 1993;Silva et al 2010]. The loss of total progressive motility could be owed to epididyimal corticosterone-induced ROS overproduction and lipid peroxidation [Dhanabalan et al 2010].…”

Section: Figure 8 Sperm Viability (A) Concentration (B) Total Spermentioning

confidence: 99%

Intrinsic and extrinsic apoptotic pathways are involved in rat testis by cold water immersion-induced acute and chronic stress

Juárez-Rojas

García-Lorenzana²,

Martínez

et al. 2015

Systems Biology in Reproductive Medicine

View full text Add to dashboard Cite

Testicular apoptosis is activated by stress, but it is not clear which signaling pathway is activated in response to stress. The aim of this study was to investigate whether intrinsic, extrinsic, or both apoptotic signaling pathways are activated by acute and chronic stress. Adult male rats were subjected to cold water immersion-induced stress for 1, 20, 40, and 50 consecutive days. The seminiferous tubules:apoptotic cell ratio was assayed on acute (1 day) and chronic (20, 40, 50 days) stress. Apoptotic markers, including cleaved-caspase 3 and 8, the pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins were also determined after acute and chronic stress induction. Additionally, epididymal sperm quality was evaluated, as well as corticosterone and testosterone levels. An increase in tubule apoptotic cell count percentage after an hour of acute stress and during chronic stress induction was observed. The apoptotic cells rate per tubule increment was only detected one hour after acute stress, but not with chronic stress. Accordingly, there was an increase in Bax, cleaved caspase-8 and caspase-3 proapoptotic proteins with a decrease of anti-apoptotic Bcl-2 in both acutely and chronically stressed male testes. In addition, sperm count, viability, as well as total and progressive motility were low in chronically stressed males. Finally, the levels of corticosterone increased whereas testosterone levels decreased in chronically stressed males. Activation of the extrinsic apoptotic pathway was shown by cleaved caspase-8 increase whereas the intrinsic apoptotic pathway activation was determined by the increase of Bax, along with Bcl-2 decrease, making evident a cross-talk between these two pathways with the activation of caspase-3. These results suggest that both acute and chronic stress can potentially activate the intrinsic/extrinsic apoptosis pathways in testes. Chronic stress also reduces the quality of epididymal spermatozoa, possibly due to a decrease in testosterone.

show abstract

“…Apparently, the classic GRs are involved in these glucocorticoid actions. Leydig cells express classic GRs [19][20][21]. The Leydig cell responds to glucocorticoids.…”

Section: Stress and Leydig Cell Functionmentioning

confidence: 99%

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Lian

Lin

et al. 2008

Steroids

View full text Add to dashboard Cite

Stress-mediated elevations in circulating glucocorticoid levels lead to corresponding rapid declines in testosterone production by Leydig cells in the testis. In previous studies we have established that glucocorticoids act on Leydig cells directly, through the classic glucocorticoid receptor (GR), and that access to the GR is controlled prior to the GR by a metabolizing pathway mediated by the type 1 isoform of 11β-hydroxysteroid dehydrogenase (11βHSD1). This enzyme is bidirectional (with both oxidase and reductase activities) and in the rat testis is exclusively localized in Leydig cells where it is abundantly expressed and may catalyze the oxidative inactivation of glucocorticoids. The predominant reductase direction of 11βHSD1 activity in liver cells is determined by an enzyme, hexose-6-phosphate dehydrogenase (H6PDH), on the luminal side of the smooth endoplasmic reticulum (SER). Generation of the pyridine nucleotide cofactor NADPH by H6PDH stimulates the reductase direction of 11βHSD1 resulting in increased levels of active glucocorticoids in liver cells. Unlike liver cells, steroidogenic enzymes including 17β-hydroxysteroid dehydrogenase 3 (17βHSD3) forms the coupling with 11βHSD1. Thus the physiological concentrations of androstenedione serve as a substrate for 17βHSD3 utilizing NADPH to generate NADP+, which drives 11βHSD1 in Leydig cells primarily as an oxidase; thus eliminating the adverse effects of glucocorticoids on testosterone production. At the same time 11βHSD1 generates NADPH which promotes testosterone biosynthesis by stimulating 17βHSD3 in a cooperative cycle. This enzymatic coupling constitutes a rapid mechanism for modulating glucocorticoid control of testosterone biosynthesis. Under stress conditions, glucocorticoids also have rapid actions to suppress cAMP formation thus to lower testosterone production.

show abstract

Localization of the glucocorticoid receptor in testis and accessory sexual organs of male rat

Cited by 94 publications

References 28 publications

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Intrinsic and extrinsic apoptotic pathways are involved in rat testis by cold water immersion-induced acute and chronic stress

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Contact Info

Product

Resources

About