Mol Hum Reprod. 2013 Jul 26;
Stojkov NJ, Baburski AZ, Bjelic MM, Sokanovic SJ, Mihajlovic AI, Drljaca DM, Janjic MM, Kostic TS, Andric SA
The molecular mechanism of stress-associated reproductive dysfunction is complex and largely unknown. This study was designed to systematically analyze molecular effects of systemic in vivo blockade of ?1-adrenergic receptors (?1-ADRs) on stress-induced disturbance of cAMP/cGMP signaling in testosterone-producing Leydig cells using the following parameters (1) level of circulating stress hormones, LH & testosterone; (2) level of main molecular markers of Leydig cells functionality (testosterone, Insl3, cAMP); (3) expression of cAMP signaling (cAMP "producers"/"effectors"/"removers"); (4) expression of NO-cGMP signaling (NO-cGMP "producers"/"effectors"/"removers"). The results showed that oral administration of ?1-ADRs blocker before stress increased cGMP and diminished stress-reduced cAMP production in Leydig cells. In the same cells, stress-induced effects on cAMP/cGMP signaling pathways elements were changed. Sustained in vivo ?1-ADRs blockade completely abolished stress-increased transcription of most abundantly expressed phosphodiesterase that remove cAMP (Pde4b) and potentiated stress-increased expression of PRKA, the main stimulator of Leydig cells steroidogenesis. In the same Leydig cells, stress-decreased NOS3 expression was abolished, while stress-increased GUCY1 (cGMP "producer") and PRKG1 (cGMP "effector") were potentiated. It is possible that all molecules mentioned could contribute, at least in part, in recovery of Leydig cells testosterone production. Presented data provide new role of ?1-ADRs in stress-triggered disturbance of cAMP/cGMP signaling, and new molecular insights into the relationship between stress and mammalian reproduction. Regardless of whether the effects of ?1-blocker+stress are direct or indirect, the results are important in terms of human reproductive health and the wide use of ?1-ADRs antagonists, alone or in combination, to treat posttraumatic stress disorders, hypertension, benign prostatic hyperplasia symptoms and potential drugs for prostate cancer prevention/treatment.
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Stojkov NJ, Baburski AZ, Bjelic MM, Sokanovic SJ, Mihajlovic AI, Drljaca DM, Janjic MM, Kostic TS, Andric SA
The molecular mechanism of stress-associated reproductive dysfunction is complex and largely unknown. This study was designed to systematically analyze molecular effects of systemic in vivo blockade of ?1-adrenergic receptors (?1-ADRs) on stress-induced disturbance of cAMP/cGMP signaling in testosterone-producing Leydig cells using the following parameters (1) level of circulating stress hormones, LH & testosterone; (2) level of main molecular markers of Leydig cells functionality (testosterone, Insl3, cAMP); (3) expression of cAMP signaling (cAMP "producers"/"effectors"/"removers"); (4) expression of NO-cGMP signaling (NO-cGMP "producers"/"effectors"/"removers"). The results showed that oral administration of ?1-ADRs blocker before stress increased cGMP and diminished stress-reduced cAMP production in Leydig cells. In the same cells, stress-induced effects on cAMP/cGMP signaling pathways elements were changed. Sustained in vivo ?1-ADRs blockade completely abolished stress-increased transcription of most abundantly expressed phosphodiesterase that remove cAMP (Pde4b) and potentiated stress-increased expression of PRKA, the main stimulator of Leydig cells steroidogenesis. In the same Leydig cells, stress-decreased NOS3 expression was abolished, while stress-increased GUCY1 (cGMP "producer") and PRKG1 (cGMP "effector") were potentiated. It is possible that all molecules mentioned could contribute, at least in part, in recovery of Leydig cells testosterone production. Presented data provide new role of ?1-ADRs in stress-triggered disturbance of cAMP/cGMP signaling, and new molecular insights into the relationship between stress and mammalian reproduction. Regardless of whether the effects of ?1-blocker+stress are direct or indirect, the results are important in terms of human reproductive health and the wide use of ?1-ADRs antagonists, alone or in combination, to treat posttraumatic stress disorders, hypertension, benign prostatic hyperplasia symptoms and potential drugs for prostate cancer prevention/treatment.
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