Absence of LHRH effect on testosterone production by Leydig cells from fetal mouse testis

1986 ◽  
Vol 24 (1) ◽  
pp. 307-310 ◽  
Author(s):  
G. Pointis ◽  
M.T. Latreille
2011 ◽  
Vol 25 (8) ◽  
pp. 1542-1547 ◽  
Author(s):  
Abdelali Lehraiki ◽  
Cathie Chamaillard ◽  
Andrée Krust ◽  
René Habert ◽  
Christine Levacher

2013 ◽  
Vol 305 (2) ◽  
pp. E194-E204 ◽  
Author(s):  
Natasa J. Stojkov ◽  
Marija M. Janjic ◽  
Aleksandar Z. Baburski ◽  
Aleksandar I. Mihajlovic ◽  
Dragana M. Drljaca ◽  
...  

This study was designed to systematically analyze and evaluate the effects of in vivo blockade of α1-adrenergic receptors (α1-ADRs) on the stress-induced disturbance of steroidogenic machinery in Leydig cells. Parameters followed 1) steroidogenic enzymes/proteins, transcription factors, and cAMP/testosterone production; 2) the main hallmarks of stress (epinephrine, glucocorticoids); and 3) transcription profiles of ADRs and oxidases with high affinity to inactivate glucocorticoids. Results showed that sustained blockade of α1-ADRs prevented stress-induced 1) decrease of the transcripts/proteins for main steroidogenic CYPs (CYP11A1, CYP17A1); 2) decrease of Scarb1 and Hsd3b1 transcripts; 3) decrease of transcript for Nur77, one of the main activator of the steroidogenic expression; and 4) increase of Dax1 and Arr19, the main steroidogenic repressors in Leydig cells. In the same cells, the expression of steroidogenic stimulatory factor Creb1, StAR, and androgen receptor increased. In this signaling scenario, stress-induced stimulation of Adra1a/Adra1b/Adrbk1 and Hsd11b2 (the unidirectional oxidase with high affinity to inactivate glucocorticoids) was not changed. Blockade additionally stimulated stress-increased transcription of the most abundantly expressed ADRs Adra1d/Adrb1/Adrb2 in Leydig cells. In the same cells, stress-decreased testosterone production, the main marker of Leydig cells functionality, was completely prevented, while reduction of cAMP, the main regulator of androgenesis, was partially prevented. Accordingly, the presented data provide a new molecular/transcriptional base for “fight/adaptation” of steroidogenic cells and new molecular insights into the role of α1-ADRs in stress-impaired Leydig cell steroidogenesis. The results are important in term of wide use of α1-ADR selective antagonists, alone/in combination, to treat high blood pressure, nightmares associated with posttraumatic stress disorder, and disrupted sexual health.


2017 ◽  
Vol 8 (10) ◽  
pp. e3123-e3123 ◽  
Author(s):  
Min Zhang ◽  
Jiancheng Wang ◽  
Chunhua Deng ◽  
Mei Hua Jiang ◽  
Xin Feng ◽  
...  

1980 ◽  
Vol 93 (2) ◽  
pp. 250-256 ◽  
Author(s):  
M. P. de la Llosa-Hermier ◽  
C. Tertrin-Clary ◽  
M. Evrard-Herouard ◽  
Y. Colleaux ◽  
C. Hermier ◽  
...  

Abstract. Rat intestinal cells prepared from testes were incubated in the presence of different lutropin derivatives obtained by chemical modification of the amino groups. The cAMP accumulation and the testosterone biosynthesis were determined in the cell homogenates. Binding determinations were carried out by a radioligand receptor assay using tritiated methylated lutropin. The binding activities — relative to native LH — of three different derivatives obtained by reductive alkylation (methylated, ethylated and isopropylated LH) were in good agreement with the relative potencies assessed by their capacity to stimulate cAMP and testosterone production. Guanidinated LH (11 — NH2 groups modified) exhibited a binding activity and a relative potency relatively high with regard to cAMP accumulation (as compared with that of native LH). Its steroidogenic potency, however, was very low. When Leydig cells were incubated in the presence of native and guanidinated LH, the testosterone production was similar to that induced by the derivative alone, indicating that the derivative exerted a competitive inhibitory action preventing the stimulation of steroidogenesis by native LH. These results suggest that a guanidinated derivative is able to bind to the LH receptor and the complex so formed is able to be coupled with an adenylate cyclase pool (or cAMP compartment) which is not connected with the steroidogenic pathway.


Reproduction ◽  
1979 ◽  
Vol 56 (2) ◽  
pp. 653-656 ◽  
Author(s):  
J. Grinsted ◽  
A. G. Byskov ◽  
M. P. Andreasen

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