Abstract
A bulk of evidence suggests that d-aspartate (d-Asp) regulates steroidogenesis and spermatogenesis in vertebrate testes. This review article focuses on intracellular signaling mechanisms elicited by d-Asp possibly via binding to the N-methyl-d-aspartate receptor (NMDAR) in both Leydig cells, and spermatogonia. In Leydig cells, the amino acid upregulates androgen production by eliciting the adenylate cyclase-cAMP and/or mitogen-activated protein kinase (MAPK) pathways. d-Asp treatment enhances gene and protein expression of enzymes involved in the steroidogenic cascade. d-Asp also directly affects spermatogonial mitotic activity. In spermatogonial GC-1 cells, d-Asp induces phosphorylation of MAPK and AKT serine-threonine kinase proteins, and stimulates expression of proliferating cell nuclear antigen (PCNA) and aurora kinase B (AURKB). Further stimulation of spermatogonial GC-1 cell proliferation might come from estradiol/estrogen receptor β (ESR2) interaction. d-Asp modulates androgen and estrogen levels as well as the expression of their receptors in the rat epididymis by acting on mRNA levels of Srd5a1 and Cyp19a1 enzymes, hence suggesting involvement in spermatozoa maturation.
Highlights
The regulation of steroidogenesis and spermatogenesis involves a complex interaction of a diversity of hormones and intracellular signaling pathways [1,2,3]
A bulk of evidence suggests that D-aspartate (D-Asp) regulates steroidogenesis and spermatogenesis in vertebrate testes
This review article focuses on intracellular signaling mechanisms elicited by D-Asp possibly via binding to the N-methyl-D-aspartate receptor (NMDAR) in both Leydig cells, and spermatogonia
Summary
The regulation of steroidogenesis and spermatogenesis involves a complex interaction of a diversity of hormones and intracellular signaling pathways [1,2,3]. Several studies reported that exogenous D-Asp administration increased T levels, the effect of the amino acid on the release of other sex steroid hormones may vary between species and between in vitro and in vivo test systems. Sicula), D-Asp concentration in the testis showed significant variations during the reproductive cycle, with the highest levels in sexually active animals [18,19,20]. There is evidence that in Leydig cells the amino acid modulates steroidogenesis by eliciting the adenylate cyclase-cAMP and/mitogen-activated protein kinase (MAPK; more commonly known as ERK, extracellular signal-regulated kinase) pathways [4]. We review intracellular signaling pathways affected by D-Asp in the testis, with focus on Leydig cells and spermatogonia
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