Abstract
Leydig cells secrete testosterone, which is essential for male fertility and reproductive health. Stress increases the secretion of glucocorticoid (corticosterone, CORT; in rats), which decreases circulating testosterone levels in part through a direct action by binding to the glucocorticoid receptors (NR3C1) in Leydig cells. The intratesticular CORT level is dependent on oxidative inactivation of glucocorticoid by 11β-hydroxysteroid dehydrogenase 1 (HSD11B1) in Leydig cells. In the present study, we investigated the time-course changes of steroidogenic gene expression levels after acute immobilization stress in rats. The plasma CORT levels were significantly increased 0.5, 1, 3 and 6 h after immobilization stress, while plasma testosterone levels were significantly reduced 3 and 6 h, after stress and luteinizing hormone (LH) did not change. Immobilization stress caused the down-regulation of Scarb1, Star and Cyp17a1 expression levels in the rat testis starting at the first hour of stress, ahead of the significant decreases of plasma testosterone levels. Other mRNA levels, including Cyp11a1, Hsd3b1 and Hsd17b3, began to decline after 3 h. Hsd11b1 and Nos2 mRNA levels did not change during the course of stress. Administration of glucocorticoid antagonist RU486 significantly restored plasma testosterone levels. In conclusion, Scarb1, Star and Cyp17a1 expression levels are more sensitive to acute stress, and acute immobilization stress causes the decline of the steroidogenic pathway via elevating the levels of glucocorticoid, which binds to NR3C1 in Leydig cells to inhibit steroidogenic gene expression.
Highlights
Leydig cells secrete the male steroid hormone, testosterone, which stimulates differentiation of the male phenotype and spermatogenesis in the testes
The average values of plasma CORT in the control rats had no significant changes between groups (Figure 1A)
During the course of immobilization stress, plasma CORT levels in the stressed rats were significantly increased 0.5, 1, 3 and 6 h (p < 0.001) after being restrained in the mesh compared to the control rats (the CORT value at 0 h = 92.02 ± 23.83 ng/mL, mean ± SEM, Figure 1A), indicating that these rats were under stress 0.5, 1, 3 and 6 h after being in the mesh
Summary
Leydig cells secrete the male steroid hormone, testosterone, which stimulates differentiation of the male phenotype and spermatogenesis in the testes. Leydig cells are one of two cell types specialized for the synthesis of steroids, the other being the adrenocortical cells of the adrenal gland. The steroid biosynthetic pathways in both glands use a common precursor, cholesterol. Cholesterol in lipoprotein-bound form is transported via scavenger receptor class B member 1 Scarb1) into both cells, where cholesterol is released. In the Leydig cell, after stimulation by luteinizing hormone (LH), cholesterol is mobilized to the inner mitochondrial membrane by the steroidogenic acute regulatory protein (StAR, encoded by Star) [1], where it is converted to the 21-carbon steroid, pregnenolone, by cytochrome P450 side chain cleavage enzyme (CYP11A1, encoded by Cyp11a1).
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