17β‐estradiol induces spermatogonial proliferation through mitogen‐activated protein kinase (extracellular signal‐regulated kinase 1/2) activity in the lizard (Podarcis s. sicula)

Abstract

There are always more evidences indicating that 17beta-estradiol (E(2)) is necessary for normal male fertility. We have used a nonmammalian vertebrate model (the lizard Podarcis s. sicula) to investigate the regulation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) activity in the testis during the annual sexual cycle and to study whether E(2) exerts a role in the spermatogenesis through ERK1/2 activity. Immunocytochemistry analysis shows that ERK1/2 proteins are present in the nucleus of the spermatogonia (SPG), and in primary (I) spermatocytes (SPC). The annual E(2) profile shows a progressive increase during the active spermatogenesis (from April to June) and a peak in the month of August (spermatogonial mitosis). In parallel, ERK1/2 (molecular weight 44 and 42 kDa, respectively) are highly phosphorylated during the period of active spermatogenesis and in post-refractory period (August) compared with the winter stasis (from November to March). Present results demonstrate that E(2) treatment induces spermatogonial proliferation, possibly via the activation of ERK1/2, and this effect is counteracted by the antiestrogen ICI 182-780.

P450 aromatase: a key enzyme in the spermatogenesis of the Italian wall lizard, Podarcis sicula

“…Indeed, the presence of such a receptor was recorded within the Sertoli and germ cells of lizard testes (Chieffi and Varriale, 2004), as well as in mammalian testes (Carreau et al, 2006). Then, estrogen receptor beta activates kinases Akt-1 (Russo et al, 2005) and ERK 1/2 (Chieffi et al, 2002), which, through the phosphorylation of transcription factors, activate the proliferation and differentiation of germ cells present in the lizard testis.…”

17β-Estradiol induces Akt-1 through estrogen receptor-β in the frog (Rana esculenta) male germ cells

“…Correct proliferation and apoptosis is required to regulate the size of cell lineages and the timing of differentiation (Matsui 1998, Chaganti & Houldsworth 2000. In vertebrates, germ-cell proliferation seems to depend on a network of factors interacting locally, such as stem-cell factor, c-kit receptor (Sorrentino et al 1991, Munsie et al 1997, platelet-derived growth factor (Li et al 1997), and E 2 (Chieffi et al 2000b(Chieffi et al , 2002. Further studies are needed to clarify the signal transduction pathways involved in their activation and the downstream targets of their action.…”

Environmental influence on testicular MAP kinase (ERK1) activity in the frogRana esculenta

“…In testicular germ cells ERKs are predominantly confined to the nuclei, where they might also regulate gene transcription and substrate phosphorylation which, in turn, regulate cell proliferation (Chieffi et al, 2000(Chieffi et al, , 2002. Since changes in the state of activation of ERKs also correlate with spermatogenetic activity, it is likely that these enzymes play a key role in the regulation of the testicular epithelium proliferation (Chieffi et al, 2000b).…”

“…Recent evidence also suggests that these otherwise distinct pathways may interact in promoting mitosis of spermatogonial stem cells (Chieffi et al, 2000b(Chieffi et al, , 2002.…”

“…ERKs are expressed ubiquitously and closely related to the yeast protein kinases involved in pheromone induced mating (Nielsen et al, 1993). For example, in the frog R. esculenta and in the lizard Podarcis s. sicula testis different levels of ERK1/2 activity are present during the annual reproductive cycle (Chieffi et al, 2001(Chieffi et al, , 2002; in addition, it has been shown that 17-β estradiol induces ERKs phoshorylation in frog (R. esculenta) (Chieffi et al, 2000b) and lizard (P. s. sicula) testis (Chieffi et al, 2002), and JNK1 has different activity in frog (R. esculenta) (Chieffi, 2003) and lizard (P. s. sicula) testis during the annual reproductive cycle (Chieffi et al, 1999). Recent studies suggest a role for ERK1 in the regulation of spermatogonial proliferation.…”